Professional Documents
Culture Documents
OULU 2007
D 908
D 908
ACTA
UNIVERSITY OF OULU P.O. Box 7500 FI-90014 UNIVERSITY OF OULU FINLAND
ACTA
U N I V E R S I T AT I S O U L U E N S I S
D
A C TA U N I V E R S I TAT I S O U L U E N S I S
S E R I E S E D I T O R S
Miia Metsänen MEDICA
Miia Metsänen
Professor Mikko Siponen
CTECHNICA
Professor Juha Kostamovaara
A STUDY OF HIGH-RISK AND LOW-RISK ADOPTEES
DMEDICA
Professor Olli Vuolteenaho
IN THE FINNISH ADOPTIVE FAMILY STUDY OF
SCHIZOPHRENIA
ESCIENTIAE RERUM SOCIALIUM
Senior Assistant Timo Latomaa
FSCRIPTA ACADEMICA
Communications Officer Elna Stjerna
GOECONOMICA
Senior Lecturer Seppo Eriksson
EDITOR IN CHIEF
Professor Olli Vuolteenaho
EDITORIAL SECRETARY
Publications Editor Kirsti Nurkkala FACULTY OF MEDICINE,
DEPARTMENT OF PSYCHIATRY,
UNIVERSITY OF OULU;
ISBN 978-951-42-8331-4 (Paperback) DEPARTMENT OF PSYCHIATRY,
ISBN 978-951-42-8332-1 (PDF) OULU UNIVERSITY HOSPITAL;
ISSN 0355-3221 (Print) CLINIC OF PSYCHIATRY,
ISSN 1796-2234 (Online) PÄIJÄT-HÄME CENTRAL HOSPITAL
ACTA UNIVERSITATIS OULUENSIS
D Medica 908
MIIA METSÄNEN
THOUGHT DISORDER AS
A PREDICTIVE SIGN OF
MENTAL DISORDER
A study of high-risk and low-risk adoptees in
the Finnish Adoptive Family Study of Schizophrenia
O U L U N Y L I O P I S TO, O U L U 2 0 0 7
Copyright © 2007
Acta Univ. Oul. D 908, 2007
Supervised by
Docent Karl-Erik Wahlberg
Docent Outi Saarento
Reviewed by
Docent Risto Antikainen
Docent Eila Laukkanen
Cover design
Raimo Ahonen
Abstract
Early recognition of schizophrenia could lead to a better clinical course and a better prognosis.
Therefore, researchers have started to investigate the possible vulnerability markers of schizophrenia.
Both genetic and environmental factors have been found to be essential in the understanding of the
development of psychiatric disorders.
The present study is part of an extensive Finnish adoptive family study of schizophrenia. The
substudies of this thesis focused on investigating the predictive value of thought disorder measured
by Thought Disorder Index (TDI) in terms of the future psychiatric disorders of adoptees at high risk
(HR, biological mother with a diagnosis of schizophrenia or paranoid psychosis) and low risk (LR,
biological mother with no diagnosed psychosis) for schizophrenia, who had no psychiatric diagnosis
at the initial assessment (n = 171). The adoptees' psychiatric status was first re-assessed based on the
DSM-III-R criteria in a re-interview 11 years later and then based on the available national hospital
discharge registers 16 years later. The predictive value of thought disorder as a sign of vulnerability
to mental disorder was clarified by examining the stability of thought disorder (n = 158). The
adoptees' TDI scores were evaluated twice at a median interval of 12 years (the adoptees' median ages
at evaluation were 22 and 36 years). Furthermore, the possible genotype-environment effect in the
development of thought disorder was investigated by assessing the adoptees' thought disorders at the
initial and follow-up assessments as well as the CD (Communication Deviance) of their adoptive
parents at the initial assessment (n = 89).
High scores on several TDI variables at the initial assessment were shown to predict a follow-up
diagnosis of a psychiatric disorder among all adoptees. These TDI variables were found to be stable
over time, which enhanced the predictive value of thought disorder. There was an association
between the thought disorder of the adoptees and the CD of their parents. Furthermore, the genotype
- environment interactions were also related to the presence of thought disorder.
The results of these investigations provide new information to the prevention of mental disorders,
especially among person with prodromal symptoms of psychosis, such as mood disorders and
cognitive dysfunctions.
Tiivistelmä
Skitsofrenian varhaisen tunnistamisen myötä saattaa olla mahdollista kohentaa skitsofrenian
ennustetta. Siksi tutkijat selvittävät mahdollisia skitsofreniaan altistavia ja ennakoivia tekijöitä. Sekä
geneettiset että ympäristöstä johtuvat tekijät ovat nousseet olennaisiksi seikoiksi psykiatristen
häiriöiden kehittymisen ymmärtämisessä.
Tämä tutkimus on osa laajempaa Suomalaista adoptiolapsitutkimusta. Tutkimuksen tavoitteena
oli selvittää ennustavatko Thought Disorder Index -asteikolla (TDI) mitatut ajatushäiriöt
tutkimushetkellä oireettomien (eivät täyttäneet psykiatrisen diagnoosin kriteereitä) riski (biologinen
äidillä skitsofrenia tai paranoidinen psykoosi diagnoosi)- ja verrokkiadoptiolasten (biologisella
äidillä ei psykoosi diagnoosia) tulevaa mielenterveyttä (n = 171). Adoptiolasten psykiatrinen status
arvioitiin 11 vuotta myöhemmin tehdyssä seurantatutkimuksessa DSM-III-R -kriteeristöllä ja tämän
jälkeen vielä seuraamalla 16 vuotta kansallisia sairaaloiden uloskirjoitusrekistereitä. Ajatushäiriöiden
ennustearvoa toimia haavoittuvuusindikaattoreina selvitettiin tutkimalla ajatushäiriöiden pysyvyyttä
(n = 158). Adoptiolasten TDI pisteet arvioitiin kahdesti heidän ollessa 22- ja 36-vuotiaita,
tutkimuksen alussa ja 12 vuoden (mediaani) seuranta-ajan jälkeen. Lisäksi mahdollista perimä-
ympäristötekijöiden yhdysvaikutusta ajatushäiriöiden kehittymisessä tutkittiin arvioimalla
adoptiolasten adoptiovanhempien kommunikaatiohäiriöt (CD) alkututkimuksessa ja adoptiolasten
ajatushäiriöt sekä alku- että seurantatutkimuksessa (N = 89).
Eräät alkututkimuksessa mitatut kohonneet TDI-muuttujat (TDR = TDI-astekon
kokonaispistemäärä, 0.50 vakavuusaste ja omituinen sanojen käyttö) ennustivat seurannassa
adoptiolasten psykiatrisen diagnoosin kriteerien täyttymistä. Kyseiset TDI-muuttujat olivat myös
pysyviä ja täten niiden ennustearvo vahvistui. Adoptiolasten ajatushäiriöiden kehittyminen alku- ja
seurantatutkimuksen välillä oli yhteydessä alkututkimuksessa mitattuun adoptiovanhempien
kommunikaatiohäiriöiden esiintyvyyteen ja perimän ja ympäristön yhdysvaikutus tuli esille.
Tämän tutkimuksen tulokset tuovat uutta tietoa ennaltaehkäisevälle mielenterveystyölle,
erityisesti niiden henkilöiden kohdalla, joilla esiintyy joitakin huolestuttavia, erityisesti psykoosin
ennakko-oireita kuten mieliala-oireita ja kognitiivisia muutoksia.
Thought disorder has been a familiar term in psychiatry ever since Emil Kraepelin
(1896/1919) and Eugen Bleuler (1911/1950, 1924) identified thinking problems as one of
the primary features of schizophrenia. However, psychiatric researchers have not reached
full consensus as to the definition of thought disorder. Kraepelin (1896/1919) identified
the incoherence and “derailments” of thought sequences in schizophrenia, while Bleuler
(1911/1950) emphasized the splitting of thoughts and feelings and called this process
“loosening of associations”. Other early theorists, such as Storch (1924) and Werner
(1957), believed primitive language usage to be characteristic of schizophrenic patients.
Correspondingly, Goldstein (1944) and Arieti (1974) viewed schizophrenic thinking on
the concrete-abstract continuum. Goldstein (1944), Arieti (1974), and Barison (1949)
characterized thought processes in schizophrenia as concrete, while Barison (1949) found
schizophrenic thinking to be overly abstract. Cameron (1944) considered the thinking
problems in schizophrenia to be due to an inability to maintain conceptual boundaries, in
accordance with Fish (1962), who defined thought disorder as a disturbance of
conceptual thinking. Von Domarus (1944) added to the conceptualization of thought
disorder the idea of predicative thinking, which means that two things are identified on
the basis of a common predicate rather than on the basis of a common subject. Some
psychoanalytically orientated scholars viewed schizophrenic thinking as the
manifestation of the primary process, representing a regression to an earlier, infantile
state of psychic development (Johnston & Holzman 1979), while Harrow and Quinlan
(1985) regarded thought disorder as consisting of diverse types of verbalization and
thinking labeled by others as bizarre and idiosyncratic. Today, thought disorder is
considered a broader phenomenon, including not only impaired pace and flow of
associations, but also errors in syntax, word usage, syllogistic reasoning, inappropriate
levels of abstracting, failure to maintain conceptual boundaries, and breakdown of the
discrimination of internal from external perceptions (Kleiger 1999).
21
Although psychiatric researchers have not reached agreement concerning the definition of
thought disorder, it is widely accepted that language and speech provide the structure
through which thought is communicated (Harrow & Quinlan 1985, Lanin-Kettering &
Harrow 1985, Holzman et al. 1986). Numerous studies have investigated the cognitive
and neurological substrate of thought disorder. Impairments in attention, information
processing, working memory, discourse planning, and semantic processing have been
found to be related to thought disorders in schizophrenia (Nuechterlein & Dawson 1984,
Hoffman et al. 1986, Liddle 1987, Manschreck et al. 1991, Shenton et al. 1992, Goldberg
et al. 1998, Nestor et al. 1998, Tallent et al. 2001, Minassian et al. 2004, Leeson et al.
2005). It has been suggested that, because of a deficit in working memory, schizophrenic
patients lose their train of thought, fail to perceive causal relationships, and are unable to
regulate their behavior by internal schemata and ideas (Goldman-Rakic 1992).
Impairments in different aspects of executive function have also turned out to be related
to thought disorder (McGrath 1991, Goldstein et al. 2002, Kerns & Berenbaum 2003,
Dixon et al. 2004, Covington et al. 2005). For example, poor planning could make an
individual unable to focus on a topic and thereby give rise to a loss of goal.
Studies concerning the pathophysiology of thought disorder have concluded that there
are multiple brain areas and/or miscommunication between brain areas producing
disturbed thinking (Friston 1998, Andreasen et al. 1999). Studies of brain morphology
have found that, especially among schizophrenic patients, the degree of reduced or
reversed lateralization of the posterior superior temporal gyrus is associated with the
severity of thought disorder (Shenton et al. 1992, Rossi et al. 1994, Petty et al. 1995,
Hirayasu et al. 1998, Rajarethinam et al. 2000, Kircher et al. 2002). High degrees of
thought disorder have also been accompanied by significant activations in the fusiform
gyrus and precuneus (Erkwoh et al. 2002). Kircher et al. (2001) further found the severity
of positive thought disorder to correlate inversely with the level of activity in the
Wernicke area.
In summary, previous studies concerning the cognitive background of thought disorder
have produced different results on what is essential in thought disorder. However, the
evaluation of these studies is quite challenging because of their marked diversity.
Different studies have used different methods, and sample sizes have not always been
very large. It could be presumed that, especially in studies of pathophysiology,
technological development could offer more sophisticated methods in the future and thus
enable more precise results.
Schizophrenia research has made a general distinction between positive and negative
symptoms. This differentiation has also been applied to thought disorder. Positive thought
disorder includes unusual ideas, delusions, and hallucinations and is commonly flagrantly
apparent as bizarreness of speech and logic (Kleiger 1999). Thinking affected by positive
thought disorder is not based on normal logic (Marengo & Harrow 1988).
22
Correspondingly, negative thought disorder is considered a deficit or absence of normal
functioning, such as poverty of speech and thought content (Kleiger 1999). Persons with
negative thought disorder have special difficulty in producing thoughts (Marengo &
Harrow 1988).
Extensive research made it apparent that thought disorder is not a single phenomenon
but consists of several factors. Harrow and Quinlan (1985) showed different types of
thought disorder to be present in the different phases of a psychiatric disorder. Looseness,
conceptual overinclusiveness, and fallacious logic were more often present in acute
conditions, while inability to think abstractly and excessively concrete thinking were
more prominent among chronic schizophrenic patients (Harrow & Quinlan 1985).
Johnston & Holzman (1979) found concept formation, cognitive focusing, reasoning, and
reality testing to be important components of thought disorder.
Thought disorder has turned out to be a continuous variable. Disordered thinking
appears to vary between milder forms of thought disorder and more severe thinking
problems (Harrow & Quinlan 1977, 1985; Johnston & Holzman 1979, Andreasen &
Grove 1986, Holzman et al. 1986). There is also variability within a given diagnostic
group or even within an individual, depending on the phase of the illness (Harrow &
Quinlan 1977). Positive and negative thought disorders have also been seen within one
and the same person (Pogue-Geile & Harrow 1985).
Although previous studies have used different methods to evaluate thought disorder,
their results have consistently shown that thought disorder consists of several factors and
is a continuous variable. Furthermore, the samples have included dozens of subjects in
each psychiatric disorder group.
Thought disorder has been traditionally associated with schizophrenia. The thinking and
speech of schizophrenic patients seem to be confused and disorganized and contain
idiosyncratic and peculiar phrases (Johnston & Holzman 1979, Holzman et al. 1986,
Solovay et al. 1987, Koistinen 1995). Furthermore, fluid and perseverative responses,
which seem odd and devoid of consensual meaning to the listener, have been shown to be
typical of schizophrenia (Kleiger 1999). Extremely severe thought disorders, such as
neologisms, incoherent statements, and responses merging two separate and incompatible
percepts (contamination), have been found among schizophrenic patients (Harrow &
Quinlan 1985, Koistinen 1995). The thinking of schizophrenic and schizotypal children is
also more impaired than that of normal children (Caplan et al. 1989, 1990, 2000; Caplan
1994, Tompson et al. 1997). Especially illogical thinking and loose associations were
more characteristic of schizophrenic and schizotypal children (Caplan et al. 1989, 1990).
In addition, Caplan et al. (1992) found that schizophrenic children used significantly
fewer cohesive devices to connect ideas expressed within and across sentences than
normal children. Furthermore, Makowski et al. (1997) demonstrated idiosyncratic word
usage, illogical reasoning, perceptual confusion, loss of realistic attunement to the task,
and loosely related ideas among schizophrenic adolescents. Furthermore, Docherty et al.
(2003) indicated clinically rated thought disorder to be associated with the severity of
23
positive but not negative schizophrenic symptoms. The level of thought disorder has also
been found to be significantly elevated in the relatives of persons with schizophrenia
(Johnston & Holzman 1979, Shenton et al. 1989, Hain et al. 1995, Vaever et al. 2005).
The thought processes of the first-degree relatives of schizophrenic and schizoaffective
manic patients have also been shown to be more deviant than those of normal controls
(Shenton et al. 1989, Kinney et al. 1997). In view of the large number of studies with
sample sizes ranging from 20 to 88 inpatients and outpatients with chronic and recent
schizophrenis as well schizophrenic and schizotypal children, the presence of thought
disorder in schizophrenia is convincing.
Thought disorder is present in other psychiatric disorders as well. Previous studies
have shown thought disorder in patients with obsessive-compulsive (n=15) (Lee et al.
2005), affective (n=1-48) (Dunayevich & Keck 2000, Wilcox 2000, Rubin & Arceneauz
2001, Dixon et al. 2004, Tai et al. 2004), schizoid (n=32) (Wolff et al. 1991), and
borderline personality disorders (n=51-83) (Edell 1987, Gandolfo et al. 1991).
Furthermore, thought disturbances have been found in schizotypal disorder (n=50)
(Handest & Parnas 2005) as well as in autistic (n=11-14) (Dykens et al. 1991, van deer
Gaag et al. 2005), bulimic (n=12) (Smith et al. 1991), and multiple complex
developmental disorders (n=20) (van deer Gaag et al. 2005) and in children with
attention-deficit hyperactivity disorder (ADHD) (n=13-115) (Caplan et al. 2001, van deer
Gaag et al. 2005). However, studies have revealed qualitative differences in thought
disorder, depending upon the severity of the psychopathology (Holzman et al. 1986,
Cuesta & Peralta 1993, Vaever et al. 2005). Holzman et al. (1986) showed that manic
patients (n=20) produce more often combinatory thinking, intrusions of irrelevant ideas,
and playful and humorous statements. Correspondingly, the thinking of schizophrenic
patients (n=43) involved interpenetrations of one idea into another and idiosyncratic and
peculiar words. Thought disorders among schizoaffective (n=22) and schizophrenic
patients (n=43) have been found to include many similarities and congruence (Shenton et
al. 1987). Similarly to schizophrenia, idiosyncratic verbalizations, autistic thinking, and
confusion were also present in the thinking of schizoaffective-manic patients. The
number of studies concerning thought disorder in psychiatric disorders other than
schizophrenia is large, and the sample sizes are sufficient to warrant the conclusion that
thought disorder is not unique to schizophrenia.
Although thought disorder is usually related to psychiatric disorders, it is important to
remember that the occurrence of minor cognitive slippage is possible in healthy
individuals as well. Most often, such slippage occurs during periods of anxiety or fatigue
(Solovay et al. 1987). Previous studies have shown that normal subjects (n=22) also have
thought disorders, but they are significantly less common and less severe than those seen
among psychiatric samples (Holzman et al. 1986, Solovay et al. 1987). However, it still
unknown how common thought disorders are in the normal population.
24
Thought disorder occurs most often during the acute phase of schizophrenia (Asarnow &
MacCrimmon 1982, Harrow et al. 1982, Marengo & Harrow 1997). Some patients
continue to have thought disorder after the acute phase, while improvements in specific
areas of thought disorder occur. Overall, thought disorders have been found to be rather
stable among schizophrenic patients (Adair & Wagner 1992, Earle-Boyer et al. 1986,
Marengo & Harrow 1988). Marengo & Harrow (1997) studied thought disorder in
schizophrenia, schizoaffective disorder, and other psychotic and non-psychotic disorders
at 2, 4.5, and 7.5 years after index hospitalization and found the stability of thought
disorder to be most prominent in schizophrenia (correlations of 0.42-0.47, depending on
the length of follow-up). In other psychiatric disorders, contrariwise, stability was quite
low and thought disorders did not persist throughout the follow-up period. Adair &
Wagner (1992) also found that the group mean of unusual verbalization (UV) scores
among schizophrenic patients did not significantly change during 6.4 years of follow-up.
The correlations were, however, modest at best (r= 0.16-0.50). Negative thought disorder
turned out to be relatively consistent in schizophrenics after 10 days’ acute admission, but
less consistent in manic patients (Earle-Boyer et al. 1986). Docherty et al. (2003) also
found moderate (r=0.48) consistency of formal thought disorder during 9-month follow-
up of schizophrenic patients. Correspondingly, Andreasen & Grove (1986) showed that
most types of thought disorder remitted in manic patients during 6 months of follow-up,
but persisted in schizophrenics, while patients with schizoaffective disorder also showed
substantial improvement of thought disorder.
It appears that thought disorder is a trait in some subgroups of schizophrenic and
manic patients (Braff et al. 1988, Harvey et al. 1990). The presence of thought disorder
after the resolution of an acute psychotic episode appears to be a powerful predictor of
poor outcome (Norman et al. 1999). However, it is also suggested that thought disorder in
psychiatric patients could have both trait and state features (depending on the context)
(Holzman 1986, Ragin & Oltmanns 1986). In healthy individuals, the presence of thought
disorder is assumed to be more a state-like feature. However, some “thinking problem”
subscales measuring communication deviance (CD) have shown certain stability among
adult subjects (r=0.29-0.35) but not among subjects aged 20 years or younger (Wahlberg
et al. 2001). As stated before, the presence of thought disorder could be a sign of
vulnerability to schizophrenia. Furthermore, previous studies have indicated that patients
with thought disorder had a poorer outcome in the future (Harrow et al. 1983, Jorgensen
& Aagaard 1988).
In summary, thought disorder has been found to have both trait and state-like features.
It is noticeable that the stability of thought disorder has not been a very popular topic of
research. Only a few studies have been made, and the follow-up times have not been very
long.
25
The concept of communication deviance (CD) was outlined by Wynne and Singer
(Wynne & Singer 1963a, b; Singer & Wynne 1965a, b). CD was defined as an unusual
way of perceiving, talking about, and reasoning about the world. The presence of CD
leaves the listener uncertain, puzzled, and unable to share a focus of attention with the
speaker. Parental CD is a relatively stable (Wahlberg et al. 2001) and enduring
“environmental” stressor during the child’s development.
CD has been found to be a heterogeneous phenomenon involving both perceptual-
cognitive disturbance and disturbance of linguistic-verbal reasoning (Miklowitz &
Stackman 1992). Wynne & Singer (1963a, b) differentiated between fragmented thinking
(difficulties in attention and perception, inadequate integration of stimuli or concepts) and
amorphous thinking (vague, indefinite, perseverative, impoverished speech).
Correspondingly, Jones (1977) found factors related to primarily perceptual
distortion,and factors measuring language or speech deviance. Studies have also proposed
that the perceptual-cognitive part of CD might be largely genetically acquired (Asarnow
et al. 1988, Nuechterlein et al. 1989, Wagener et al. 1986), whereas the forms of CD
reflecting deviance in linguistic-verbal reasoning tend to be more heavily influenced by
psychosocial factors (Miklowitz & Stackman 1992).
27
Previous studies have shown Communication Deviance (CD) to have stable, trait-like
features. Doane & Mintz (1987) examined 29 schizophrenic patients and found at 15-year
follow-up that CD was relatively stable among 16 women (r= .59, p<.05). Velligan et al.
(1995) studied Interactional Communication Deviance (ICD) in a series of 24 male
schizophrenic patients and their mothers. The stability of total ICD was .64 for the male
patients and .55 for the mothers over a mean time interval of 88.8 days. Nugter et al.
(1997) investigated the stability of CD and the effect of treatments on 37 two-parent and
14 single-parent families of schizophrenic patients. Parental CD was resistant to change
over a 12-month period in both treatment groups (individual treatment group and
individual treatment plus family therapy). Wahlberg et al. (2001) also found CD to be
stable in the older (over 20 years of age) 158 participants over the 11-year interval,
Furthermore, gender, genetic risk for schizophrenia, and DSM-III-R psychiatric
28
diagnoses had no effect on this stability. The stability of CD has also been verified by
Keskitalo (2000). CD was fairly stable both temporally and from one interactive situation
to another.
Previous studies have clearly pointed out the possibility of thought disorder as one of the
signs of vulnerability to schizophrenia. Furthermore, it is known that thought disorder is
not a unique characteristic of schizophrenia but also appears in individuals with other
psychiatric disorders as well as in healthy individuals during anxiety or fatigue. However,
the predictive value of thought disorder among other psychiatric disorders has not yet
29
been studied. It has also become apparent that thought disorder has both qualitative and
quantitative aspects. More information is still needed to clarify specifically the kinds of
thought disorder that could be conclusive signs of vulnerability to mental disorders.
Furthermore, the data about the stability of thought disorder has been obtained from
studies with rather short follow-up periods. In order to study the predictive value of
thought disorder, longer follow-ups are needed.
Studies concerning the development of thinking have indicated that the child’s
thinking is a result of the interaction between the child and the parents’ communication.
Especially,parental communication deviance (CD) has been found to be an enduring
“environmental” stressor during the child’s development. The association between
thought disorder and CD also needs some clarification in the longitudinal perspective.
3 Aims of the present study
The purpose of this study was to investigate the predictive value of thought disorder
concerning subsequent psychiatric disorder (I), the stability of thought disorder (II, III),
and the association between thought disorder and Communication Deviance (CD) (IV).
The specific research questions were:
1. Could premorbid signs of thought disorder determined by TDI (Thougth Disorder
Index) predict the subsequent manifestation of psychiatric disorders (I)?
2. Are thought disorders present after a 12-year follow-up? Does the genetic liability to
schizophrenia affect the stability of thought disorder (II)?
3. Are thought disorders only stable at certain severity levels and in the presence of
certain schizophrenia factors of the Thought Disorder Index (TDI) scale? What is the
significance of genetic status and the type of psychiatric disorder for the persistence of
TDI severity levels and factors (III)?
4. Are the thought disorders of high- and low-risk adoptees associated with the
Communication Deviance (CD) of the adoptive parents in the longitudinal perspective
(IV)?
4 Materials and methods
This investigation is part of the extensive Finnish adoptive family study of schizophrenia
(389 families) (Tienari et al. 1987a, b, 1994, 2000) that focuses on gene-environment
interactions in schizophrenia. The hospital records of the 19 447 women admitted to
Finnish psychiatric hospitals from January 1, 1960 through 1979 were reviewed to
identify those with a diagnosis of a schizophrenic or paranoid psychosis. Index mothers
who had given one or more offspring up for adoption were identified through every
census and parish register in the country. Women were excluded if they had an organic
brain syndrome, severe mental retardation, primary alcoholism (preceding
schizophrenia), or any other major physical illness (Tienari et al. 1987a, b, 2000, 2003).
Once the adoptees at high risk (HR) for schizophrenia had been identified, their
adoptive parents were eligible for the study with no diagnostic exclusion criteria (Tienari
et al. 2000). Low-risk (LR) adoptees and their adoptive parents consisted of families in
which the adoptees had been adopted away by biological mothers with non-spectrum
diagnoses or no psychiatric disorder. No diagnostic exclusion criteria of either physical or
mental illness were applied to the control adoptive parents. Adoptees were excluded if
they had been adopted by a relative, adopted abroad, or adopted after the age of 4 years.
The final sample included 190 genetically high-risk (HR) offspring whose biological
mothers had verified DSM-III-R diagnoses of the broad schizophrenia spectrum (n=174
(Kendler et al. 1996, Tienari et al. 2000, 2003). The broad schizophrenia spectrum
included the following diagnoses: DSM-III-R schizophrenia, odd-cluster personality
disorders (schizotypal, schizoid, and paranoid personality disorders plus avoidant
personality disorder), nonschizophrenic nonaffective psychoses (schizoaffective,
schizophreniform, and delusional disorders and psychotic disorder not otherwise
specified), and affective psychoses (bipolar and depressive disorders with psychotic
features). The HR offspring were blindly compared with the 192 adoptees at low genetic
risk (LR) whose biological mothers had nonspectrum diagnoses or no psychiatric
disorder (n=190).
32
All available adoptees were evaluated twice. At the initial assessment the adoptees’
median ages were 26 years (IR=18-36) for the HR adoptees and 22 years (IR=17-33) for
the LR adoptees (Tienari et al. 2003). Correspondingly, the median age at the follow-up
evaluation was 44 years (IR=36-52) for the HR and 43 years (IR=37-51) for the LR
adoptees. Of the high-risk adoptees, 92 were male and 98 female, whereas 90 of the LR
adoptees were male and 102 were female (Tienari et al. 2003).
All available biological mothers and biological fathers at high risk (HR) and low risk
(LR) for schizophrenia were personally interviewed (Tienari et al. 1987a,b). The
interviewers of the biological parents were experienced psychiatrics trained in diagnostic
interviews for the Present State Examination (PSE) (Wing et al. 1974), they were
provided training, and interrater reliability checks were performed at Maudsley Hospital
in London (Tienari et al. 1987a,b). The initial and subsequent hospital and clinic records
as well as personal interviews were used to make the research diagnoses according to the
DSM-III-R. In addition, the diagnoses and the diagnostically relevant information have
been checked based on the register data available for all study subjects (Tienari et al.
2000). The parental communication patterns were also evaluated by using the Rorschach
test.
The evaluations of the adoptees’ psychiatric status and thought disorders were part of
the study. The psychiatric assessment included personal interviews, a review of possible
hospital records and registers, and interviews with family members and other informants.
A psychological evaluation, including an individual Rorschach test, was also performed.
All evaluation procedures were carried out in the adoptive families’ home.
The adoptees were independently re-examined in the same manner after a median
interval of 12 years (Interquartile range, IR=8-15). Thereafter, the adoptees’ psychiatric
diagnoses and diagnostically relevant information were followed up until the end of the
year 2000 from national health and hospital registers. The median follow-up period was
18 years (IR=15-21). The follow-up interview schedules included an expanded lifetime
version of the Present State Examination (Wing et al. 1974), the Structured Clinical
Interview for DSM-III-R Personality Disorders (Spitzer & Williams 1986), and the
Structured Interview for Schizotypy (Kendler et al. 1989).
Study sample in original publication I. The study sample included the adoptees without
any psychiatric disorder at the initial assessment who had been administered the
Rorschach test (n=171). Of these subjects, 75 were HR and 96 were LR adoptees. The
median age of the adoptees was 21 years at the initial assessment (Interquartile range,
IR=16-29) (mean=23, sd±9.2), 34 years at follow-up assessment (IR=28-43) (mean=35,
sd±9.3), and 42 years at register follow-up (IR=35-50) (mean=42, sd±9.4). Their median
age at placement in the adoptive families had been 12 months (IR=5-24) (mean=17,
33
sd±14.4). There were 90 were female and 81 male adoptees. The social status of the
adoptive families was rated by using a Finnish classification of the main provider’s
occupation and education (Handbook for Office of Statistics 17, 1983). This classification
is based on the social status of occupations. The first group included people in managerial
positions; the second included entrepreneurs, foremen, and higher officials; the third
included skilled workers and lower officials; and the fourth comprised unskilled workers.
Accordingly, 11% of the families were rated as being in social class I, 47% in class II,
37% in class III, and 5% in class IV. The median follow-up interval in this subsample was
12 years (IR=7-15) (mean=11, sd±4.1). There were no statistically significant differences
in the demographic variables (age, age at placement, gender, and social group) between
the HR and LR adoptees. A comparison of the demographic variables of the adoptees in
this subsample and in the whole sample revealed no statistically significant differences,
except in the adoptees’ age. The adoptees in this study were younger (median age=21
years, IR=16-29) than those in the whole sample, and this variable was therefore
controlled in the multivariate model (logistic regression analysis).
Study sample in original publications II-III. This subsample included the 158 adoptees
whose thought disorder had been assessed by Thought Disorder Index (TDI) both at the
baseline of the study and at follow-up. A further inclusion criterion was that the
Rorschach records had been tape-recorded and transcribed. Of these subjects, 78 were
high-risk (HR) and 80 low-risk (LR) adoptees. The median age of the adoptees was 22
years at the initial assessment (IR=17-32) (mean=25, sd±9.8) and 36 years at the follow-
up assessment (IR=31-45) (mean=37, sd±9.8). Their median age at placement in the
adoptive families was 13 months (IR=6-24) (mean=17, sd±13.4). There were 86 were
female and 72 male adoptees. The distribution of the social groups of the adoptive
families were as follows: social group I 13%, social group II 48%, social group III 32%,
and social group IV 7%. The median follow-up interval in this subsample was 12 years
(IR=8-14) (mean=11, sd±3.8). A comparison of the demographic variables of the
adoptees in this subsample and in the whole sample revealed no statistically significant
differences. The HR adoptees did have significantly more psychiatric disorders than the
LR adoptees at follow-up (p=.01; χ2 test, two-tailed significance). (II, III Table 1)
Study sample in original publication IV: This study sample included the adoptees
whose thought disorder had been assessed at both initial and follow-up evaluations by
using the Thought Disorder Index (TDI). The inclusion criterion was that the Rorschach
records had been tape-recorded and transcribed. Furthermore, the assessment of
communication deviance (CD) of both adoptive parents was relevant. Three single-parent
families who had never had an adoptive father were also included. In these cases, the CD
of the tested adoptive mother was multiplied by two to get a CD score comparable to two
parents’ combined CD score. The final subsample included 89 adoptees. Of the subjects,
38 were high-risk (HR) and 51 low-risk (LR) adoptees. The median follow-up interval in
this subsample was 13 years (IR=9-14) (mean=12, sd±3.6). The adoptees’ median age
was 18 years at the initial assessment (IR=16-23) (mean=20, sd±6.7) and 33 years at the
follow-up assessment (IR=28-37) (mean=33, sd±7.9). Their median age at placement in
the adoptive families was 12 months (IR=5-23) (mean=16, sd±13.5). There were 50
female and 39 male adoptees. The socal group distribution of the adoptive families was as
follows: social group I 9%, social group II 53%, social group III 34%, and social group
34
IV 4%. The HR adoptees had significantly more psychiatric disorders than the LR
adoptees at follow-up (p=.004; χ2 test, two-tailed significance). (IV Table 1)
4.4 Variables
The Rorschach test was used to evaluate both the adoptees’ thought disorder and the
adoptive parents’ communication patterns. The assessments were performed according to
Klopfer & Davidson (1962) and Singer & Wynne (1986) in order to evaluate the degree
of communication deviance (Appendix 1). The interview and testing sessions were tape-
recorded. and the tapes were transcribed verbatim. The psychiatrists administered the
Rorschach test with a complete set of ten cards. They were trained to do this by an
experienced clinical psychologist (Karl-Erik Wahlberg).
The Thought Disorder Index (TDI) was used to assess the adoptees’ thought disorders.
The scoring of TDI at the initial assessment was done by four experienced psychologists
(Heljä Anias-Tanner, Pekka Koistinen, Taneli Tarvainen, Karl-Erik Wahlberg) pairwise
unaware of the subjects’ relatedness to their biological and adoptive families or their
psychiatric diagnoses. They only knew the subjects’ age, sex, and occupation. The TDI
instrument has not been used before in Finland, and an enormous amount of work had to
be done to adapt the TDI questionnaire to the Finnish language and culture (Wahlberg
1994, Koistinen 1995). A procedure of detemining the reliability of the scores between
the raters was also developed. These operations were done in co-operation with Dr. P.S.
Holzman (one of the developers of the scale) and the Drs Wynne and Singer. In cases of
disagreement concerning the scoring, a consensus score was negotiated between the
psychologists (Wahlberg 1994). The scoring of TDI at follow-up was made by one
psychologist (M.Metsänen), again unaware of the subjects’ relatedness to their biological
and adoptive families and their psychiatric diagnoses. As at the initial assessment, she
only knew the subjects’ age, sex, and occupation. Furthermore, she was blind to the
ratings of the other psychologists. M. Metsänen was trained by K-E Wahlberg, P.
Koistinen, and T. Tarvainen to use the TDI scoring system. In the training process, a large
number of Rorschach records were reviewed, and the reliability study was done by using
20 records.
The communication patterns of the adoptive parents was assessed for Communication
Deviance (CD). Dr Singer and Dr Wynne trained Dr Wahlberg in the scoring of CD, and
the minor modifications of the scoring in Finnish compared to English were discussed
(Wahlberg 1994). The scoring was carried out by two psychologists (K-E. Wahlberg, P.
Keskitalo) unaware of the participants’ status in accordance with the manual of Singer
and Wynne (1986). The Finnish translation of the CD manual was also produced as team
work between the Finnish psychologists (K-E. Wahlberg, P. Keskitalo) and the Drs Singer
and Wynne (Wahlberg 1994, Keskitalo 2000).
The adoptees’ psychiatric status was assessed by psychiatrists blind to their high-
risk/low-risk status and other background information. The diagnoses were made
according to the DSM-III-R criteria (American Psychiatric Association 1987).
35
The Thought Disorder Index (TDI) identifies 23 different items weighted along a
continuum of severity (0.25, 0.50, 0.75 and 1.0) (Johnston & Holzman 1979, Solovay et
al. 1987) (Table 1). The 0.25 severity level represents minor idiosyncrasies. It is very
common that even healthy individuals make comments at the 0.25 level, especially under
anxiety or fatigue. At the 0.50 severity levels, responses indicate a loss of mooring, shaky
reality contact, emotional overreaction, and distinct oddness but are still in reality
(Solovay et al. 1986). The 0.75 level is associated with psychotic disruption and
characterized by instability of thinking and perception, absurdity, and an unrestrained
combinatory tendency (Solovay et al. 1986). The 1.0 level represents responses
completely out of reality (Solovay et al. 1986).
The developers of the TDI scale (Johnston & Holzman 1979, Holzman et al. 1986,
Solovay et al. 1986) used weighted scores, and to calculate total TDI (TDR), the
following formula was applied in this study:
where A=the number of responses scored at the level 0.25, B=the number of responses
scored at the level 0.50, C=the number of responses scored at the level 0.75, and D=the
number of responses scored at the level 1.00.
Every severity level was calculated by summing up the relevant item scores and
dividing the sums by the number of responses.
Holzman et al. (1986) constructed a set of factors from the TDI categories that
discriminated best between schizophrenic and manic patients. They were able to
construct three factors that were conceptually characteristic of schizophrenic patients:
fluid thinking, confusion, and idiosyncratic verbalization. Each factor scale was
calculated by summing up all relevant thought disorder item scores and dividing the sums
with the number of responses. Fluid thinking includes the TDI items 9 (Relationship
verbalization), 17 (Fluidity), and 21 (Contamination), confusion the items 5 (Word-
finding difficulty), 12 (Confusion), 18 (Absurd responses), and 23 (Neologisms), and
idiosyncratic verbalization item 4 (Peculiar verbalizations and responses).
36
Table 1. a) Thought Disorder Index levels and categories (I Table 1).
0.25 level 0.50 level
1. Inappropriate distance 8d. External-internal response
a. Increase of distance 9. Relationship verbalization
b. Excessive qualification 10. Idiosyncratic symbolism
c. Concreteness a. Color symbolism
d. Overspecificity b. Image symbolism
e. Syncretistic response 11. Queer responses
2. Flippant response a. Queer expressions
3. Vagueness b. Queer imagery
4. Peculiar verbalizations and responses c. Queer word usage
a. Peculiar expression 12. Confusion
b. Stilted, inappropriate expression 13. Looseness
c. Idiosyncratic word usage 14. Fabulized combinations, impossible or bizarre
5. Word-finding difficulty
6. Clangs 15. Playful combinations
7. Perseveration 16. Fragmentation
8. Incongruous combinations
a. Composite response
b. Arbitrary form-color response
c. Inappropriate activity response
Thought Disorder Index (TDI) has been found to be a valid indicator of disordered
thinking in schizophrenic patients (Holzman et al. 1986, Shenton et al. 1987, Hurt et al.
1983, Hain et al. 1995). The validity of TDI among schizophrenic patients has been
confirmed: schizophrenic patients had elevated levels of thought disorder in all categories
and at all severity levels, while normal controls demonstrated only rare instances of
disordered thinking in most domains. Furthermore, different factors have turned out
useful in distinguishing between diagnostic groups (Holzman et al. 1985, Shenton et al.
1987, Solovay et al. 1987). Studies on the reliability of TDI have reported the inter-rater
reliabilities for total TDI scores to range from 0.82 to 0.93 (Johnston & Holzman 1979,
37
Solovay et al. 1986, Coleman et al. 1993). Furthermore, Solovay et al. (1986) reported
individual scoring categories of 0.81, severity levels of 0.79, and various factor scores
ranging from 0.84 to 0.89.
In this study, the intraclass correlation (ICC) between the pairs of psychologists at the
initial assessment was 0.94 for TDR, 0.92 for 0.25 level, 0.92 for 0.50 level, 0.86 for 0.75
level, 0.66 for 1.0 level, 0.95 for fluid thinking, 0.33 for confusion, and 0.80 for
idiosyncratic verbalization (n=59). The reason for the low reliability at the 1.0 level and
in confusion was the restricted range in these categories (most subjects had 0 scores), not
frequent disagreements between the scorers. Most of the records were randomly selected
for reliability analysis, except the 15 records of schizophrenic patients. These were
included in the reliability sample to ensure that there were also records with several types
of thought disorder. Reliability was also checked (every 20. record) (n=31) at follow-up
by the single-measure ICC between the two psychologists (M. Metsänen and K-E
Wahlberg). The ICCs were 0.98 for TDR, 0.85 for 0.25 level, 0.92 for 0.50 level, 0.95 for
0.75 level, 0.83 for fluid thinking, 0.86 for confusion, and 0.49 for idiosyncratic
verbalization. The 1.0 severity level was omitted because only one subject had scores at
this level at the initial assessment.
The diagnoses of the adoptees were made according to the DSM-III-R criteria (American
Psychiatric Association 1987) based on the personal interviews (Tienari et al. 2000). The
interview schedules included an expanded lifetime version of the PSE (Wing et al. 1974),
Structural Clinical Interview for DSM-III-R Personality Disorders (SCID-II) (Spitzer et
al. 1989), and the Structured Interview for Schizotypy (SIS) (Kendler et al. 1989). The
DSM-III-R diagnoses were made according to the best estimate of the most severe
lifetime Axis I (clinical syndromes) or Axis II (developmental disorders and conditions,
personality disorders) psychiatric disorder based on all available data (psychiatric
hospital records, research interviews). Comorbid and supplementary diagnoses were also
applied. The diagnoses were made at maximum certainty, i.e. the disorder had to be
diagnosed as probable or definite. The kappa coefficient for inter-rater reliability varied
between the different raters, ranging from 0.71 to 0.80 (Tienari et al. 2000).
Original paper I: The adoptees were divided into three major diagnostic groups. The
diagnostic hierarchy of disorders was established in line with the suggestions of Kendler
et al. (1996). The first group consisted of the subjects without psychiatric disorder (No
Psychiatric Disorder, NPD) at either the initial or the follow-up assessment (n=130). The
second group (n=33) consisted of adoptees with Any Other Psychiatric Disorder (AOPD)
except the broad spectrum of schizophrenia at follow-up. The second group consisted of
borderline (3), antisocial (2), narcissistic (2), histrionic (5), and obsessive-compulsive (2)
personality disorders, personality disorder NOS (2), anxiety (6), alcohol (3), mild mood
(6), and dysthymic (2) disorders. The third group comprised subjects with Broad
Schizophrenia Spectrum Disorders (BSSD) (n=8) and included cases with schizophrenia
(1), paranoid (2), avoidant (2), and schizoid (1) personality disorders, bipolar psychosis
(1), and depressive psychosis (1). The second and third groups together constituted the
group of adoptees with Any Psychiatric Disorder (APD).
Original paper II-III: The study sample was divided into two diagnostic groups. The
first group consisted of adoptees without Any Psychiatric Disorder (No Psychiatric
Disorder, NPD) (n=87). All possible diagnoses were excluded from the NPD group in
order to study the stability of TDI in a maximally healthy sample. The second group
included adoptees with Any Psychiatric Disorder (APD) (n=87). The distribution of the
APD group was as follows: schizophrenia (3), schizotypal (1), paranoid (2), schizoid (2),
avoidant (4), antisocial (6), borderline (7), narcissistic (4), histrionic (5), dependent (2),
and obsessive-compulsive (2) personality disorders, personality disorder NOS (4), bipolar
(2), and depressive (1) psychosis, anxiety (10), alcohol (5), mild mood (7), dysthymic (5),
eating (1), somatoform (2), and other (12) psychiatric disorders.
Original paper IV. The adoptees were divided into two diagnostic groups. The first
group included adoptees without any psychiatric disorder (NPD; at the initial assessment
n=74, at follow-up n=53). The second group consisted of adoptees with any psychiatric
disorder (APD). The APD group included the adoptees with the following diagnoses at
the initial assessment (n=15): schizophrenia (1), bipolar psychosis (1), antisocial (2),
borderline (1), and dependent (2) personality disorders, personality NOS (1), anxiety
disorders (3), eating disorders (1), alcohol use (1), and dysthymic disorder (2).
Correspondingly, the distribution of the diagnoses at follow-up was as follows (n=36):
40
schizophrenia (1), paranoid (2), schizoid (1), antisocial (4), borderline (4), narcissistic
(2), histrionic (3), avoidant (2), dependent (1), and obsessive-compulsive (1) personality
disorders, personality disorder NOS (2), mild mood disorders (3), dysthymic disorder (1),
and anxiety disorders (4).
The group differences (two independent samples) in the categorical variables were
assessed with the Chi-square χ2 test or Fisher’s Exact test and those in the continuous
variables with Student’s t-test or the Mann-Whitney U-test. The differences between the
initial and follow-up assessments (two related samples) in the continuous and categorical
variables were analyzed with the pair-samples t-test and McNemar’s test, respectively
(McCullagh & Nelder 1989, Bland 1995).
Analysis of covariance (ANCOVA) was used to examine group differences in the
continuous variables after controlling for potential confounders. The Tukey-Kramer
method was used as an adjustment procedure for multiple testing in ANCOVA.
(Tabachnick & Fidell 1989). Logistic regression analysis was used to assess the statistical
significance of an association of the independent categorical and continuous explanatory
variables with the dichotomous outcome variable (Kleinbaum 1994). Receiver operating
characteristic (ROC) curve analysis was done to find the best cut-off point for each TDI
subscale (Gniner et al. 1981).
All statistical analyses were performed using the SPSS (version 9.0, 11.0, 12.0) and
the SAS version 8.2 version (SAS Institute, Cary, NC).
The Finnish Adoptive Family Study was approved by the Ethics Committee of the
Medical Faculty of the University of Oulu (Finland). The sample used in the study
already existed. Thus, there was no need to meet personally the study subjects of the
study. The ethical considerations of this study are related to the use of the achieved
results in possible preventive work in the future. Collaboration with the people at risk to
develop a psychiatric disorder at follow-up and their relatives is extremely important. The
goal of preventive work is not to control their lives but to provide ways to support their
mental health. The relatives of these persons could also learn new ways to help their
family member at risk. Furthermore, it is essential to emphasize that not all people with
risk factors eventually develop a psychiatric disorder.
41
I have been participating in the Finnish Adoptive Family Study of Schizophrenia since
2000. I have scored all follow-up TDI records, completed the reliability studies of the
follow-up TDI records, performed statistical analyses, interpreted the results, and written
all manuscripts with consultation of co-workers.
5 Results
High scores at the initial assessment were shown to be statistically significantly more
common among the adoptees with a follow-up diagnosis of ‘Any Psychiatric Disorder’
(APD, n=41) than among the adoptees with ‘No Psychiatric Disorder’ (NPD, n=130) at
follow-up on the following TDI measures: TDR (APD vs. NPD, 61% vs. 43%, χ2 test ,
df=2, p=.05), the 0.50 severity level (71% vs. 51%, χ2 test , df=2, p=.03), and
idiosyncratic verbalization (63% vs. 40%, χ2 test , df=2, p=.01) (I Table 2). These
differences were especially prominent in a comparison of the adoptees with ‘Any Other
Psychiatric Disorder’(AOPD, n=33) to the NPD adoptees: TDR (AOPD vs. NPD, 64%
vs. 43%, χ2 test, p=.04), 0.50 severity level (70% vs. 51%, χ2 test, p=.05), and
idiosyncratic verbalization (61% vs. 40%, χ2 test, p=.03). No statistically significant
difference in these TDI measures was seen between the adoptees with ‘Broad
Schizophrenia Spectrum Disorder’ (BSSD, n=8) and the NPD adoptees.
The TDI scores of the high-risk (HR) adoptees were not associated with their
subsequent psychiatric status. There was, however, a tendency toward a greater
proportion of HR adoptees with high scores (as compared to low scores) at the initial
assessment to have TDR (63% vs. 37%), 0.25 severity level (95% vs. 5%), and
idiosyncratic verbalization (68% vs. 32%) among the group of AOPD adoptees observed
at follow-up. (Table 3: I Table 3; The table of the original article included a misprint in
the result of the 0.25 severity level, which has now been corrected).
43
Table 3. Percentage (%) and number (n) of high and low initial TDI variables of the
high-risk adoptees in the different groups of mental disorders (n=75)(I Table 3)
TDI variables NDPa AODPb BSSDc p-values
n=50 (67%) n=19 (25%) n=6 (8%)
% n % n % n
TDR
high 48.0 24 63.2 12 50.0 503
low 52.0 26 36.8 7 50.0 3 0.33
0.25
high 88.0 44 94.7 18 100.0 6
low 12.0 6 5.3 1 0.0 3 0.41e
0.50
high 50.0 25 57.9 11 66.7 4
low 50.0 25 42.1 8 33.3 2 0.41
0.75
high 40.0 20 47.4 9 16.7 1
low 60.0 30 52.6 10 83.3 5 1.0
fluid thinking
high 30.0 15 31.6 6 16.7 1
low 70.0 35 68.4 13 83.3 5 0.86
confusion
high 12.0 6 0.0 0 16.7 1
low 88.0 44 100.0 19 83.3 5 0.41e
idiosyncratic
verbalization
high 50.0 25 68.4 13 66.7 4
low 50.0 25 31.6 6 33.3 2 0.14
a no psychiatric disorder at the initial assessment and at follow-up
b no psychiatric disorder at the initial assessment and any other psychiatric disorder at follow-up
c no psychiatric disorder at the initial assessment and broad schizophrenia spectrum disorder at follow-up
d no psychiatric disorder at the initial assessment and any psychiatric disorder at follow-up
e Fisher’s exact test
Furthermore, 87.5% of the low-risk (LR) adoptees with a follow-up diagnosis of APD
(n=16) had high scores on the 0.50 severity level at the initial assessment, while the
respective proportion of high scores among the NPD adoptees (n=80) at follow-up was
51% (χ2 test, p=.01). This difference was especially obvious among the adoptees in the
AOPD group (n=14) (AOPD vs. NPD, 86% vs. 51%, χ2 test, p=.02). Similarly to the HR
adoptees, high scores on the TDI measures at the initial assessment were found to be
more common among the LR adoptees with a follow-up diagnosis for mental disorders (I
Table 4)
Logistic regression analysis was used to predict the follow-up psychiatric status of the
adoptees with genetic liability for schizophrenia and different TDI variables measured at
the initial assessment. The statistically significant associations are presented in Table 4.
44
Table 4. Adjusted odds ratios (OR) for different high TDI scores of the adoptees with
predictors of genetic liability for schizophrenia at the initial assessment and interaction
of TDI scores and genetic liability for any psychiatric disorder (APD) at follow-up.
Variable Adjusted 95% Confidence p
Odds Ratio* Interval
high TDR 2.20 1.06-4.58 0.04
genetic liability 3.34 1.04-10.81 0.04
interaction for TDR and genetic liability 0.61 0.13-2.86 0.53
high 0.50 severity level 2.68 1.23-5.85 0.02
genetic liability 8.87 1.72-45.63 0.01
interaction for 0.50 severity level and genetic 0.20 0.03-1.31 0.09
liability
high idiosyncratic verbalization 2.55 1.22-5.31 0.02
genetic liability 2.49 0.79-7.82 0.12
interaction for idiosyncratic verbalization and 0.87 0.19-4.04 0.86
genetic liability
* Odds ratios with 95% confidence interval from a logistic regression model predicting the likelihood for the
adoptee’s psychiatric disorder at follow-up with different TDI variables and the genetic liability for
schizophrenia (high-risk, low-risk).
The stability of the adoptees’ thought disorder between the initial and follow-up
assessments was investigated using the total TDR scores, the severity levels (0.25, 0.50
and 0.75), and schizophrenia factors (fluid thinking, confusion, idiosyncratic
verbalization) separately.
At the baseline, the variation of the total TDR score was shown to associate
statistically significantly only with female gender (ANCOVA, F-statistic = 10.52, p =
0.002), but not with any other main effects (genetic risk, psychiatric status), age at the
initial assessment, or any interactions between genetic risk, gender, and psychiatric status
(II Table 2). At follow-up, only the baseline TDR explained the variation of the total TDR
at follow-up, but none of the main effects, age at follow-up, or interaction terms did
(Table 5: II Table 3).
45
Table 5. Total TDI (TDR) scores at follow-up assessment and their association with
genetic risk, gender and psychiatric status of the adoptees. (II Table 3)
TDR at follow-up N Adj. mean (SE) ANCOVA*
for main effects F-statistic p-value
Corrected model * 158 1.28 0.25
Main effects
Genetic risk
LR 80 7.19 (0.76) 0.04 0.84
HR 78 6.97 (0.77)
Gender
Girl 86 6.55 (0.73) 0.92 0.34
Boys 72 7.61 (0.82)
Psychiatric status at follow-up
No psychiatric disorder (NPD) 71 7.44 (0.81) 0.44 0.51
Any psychiatric disorder (APD) 87 6.71 (0.74)
Interactions
Genetic risk*Gender 0.26 0.61
Genetic risk*Psychiatric status 2.86 0.09
Gender*Psychiatric status 0.02 0.89
Genetic risk*Gender*Psychiatric status 1.46 0.23
Covariates
TDR at initial assessment 5.21 0.02
Age at follow-up 1.96 0.17
* ANCOVA was used to assess the statistical significance of the mean difference in follow-up scores between
the groups (genetic risk, gender, psychiatric status) after adjustment for TDR at the initial assessment and the
adoptee’s age at follow-up and correction for multiple comparisons with the Tukey-Kramer method
The TDI scores at all TDI severity levels decreased between the initial and follow-up
assessments (III Table 2). However, stability of the scores between the initial and follow-
up assessments was seen at the 0.50 and 0.75 severity levels, but not at the 0.25 severity
level (Figure 1: III Figure 1). The adoptees’ genetic or psychiatric status was not
associated with the results (III Table 3).
46
a) The 0.25 severity level of the TDI scale
b) The 0.50 severity level of the TDI scale
5
5
4
TDI score at follow-up assessment
1
0
-1 0
-2 -1
-2 -1 0 1 2 3 4 5 -1 0 1 2 3 4 5
4
TDI score at follow-up assessment
-1
-1 0 1 2 3 4 5
Fig. 1. Relationship of the TDI scores between the initial (baseline) and follow-up assessments
at the a) 0.25, b) 0.50, and c) 0.75 severity levels of the TDI scale (III Figure 1).
Correspondingly, despite the decreased scores of all Holzman’s schizophrenia factors (III
Table 4), only idiosyncratic verbalization was shown to remain stable between the initial
and follow-up assessments, and this stability was not related to the adoptee’s genetic or
psychiatric status. (Table 6: III Table 5)
47
Table 6. Association of Holzman’s schizophrenia factors on the TDI scale between the
initial and follow-up assessments among the adoptees. (III Table 5)
Schizophrenia factors OR (95%CI) P-value
Fluid thinking
Model 1, unadjusted* 2.29 (0.87-6.05) 0.09
Model 2, adjusted ** 2.34 (0.84-6.54) 0.11
Confusion
Model 1, unadjusted 2.22 (0.43-11.56) 0.34
Model 2, adjusted 2.05 (0.38-10.99) 0.40
Idiosyncratic verbalization
Model 1, unadjusted 2.16 (1.13-4.15) 0.02
Model 2, adjusted 2.33 (1.19-4.53) 0.01
* Model 1: In each schizophrenia factor, binary logistic regression analysis (odds ratios, OR, and 95%
confidence intervals, CI) was used to assess the association between the TDI at follow-up assessment (as
outcome) and the TDI at baseline.
**Model 2: In each schizophrenia factor, binary logistic regression analysis (OR, 95% CI) was used to assess
the association between the TDI at follow-up assessment (as outcome) and the TDI at baseline after controlling
for gender, age, and genetic and psychiatric status and their interactions.
The effect of the adoptive parents’ Communication Deviance (CD) on the adoptee’s total
TDR scores was discussed in the original publication IV. The upper quartiles in the
distribution of both the adoptees’ TDR and the parents’ CD were defined as the most
deviant extremes of these variables (high TDR, high CD).
At the initial assessment, the proportion of adoptees with high TDR scores was about
twofold if the adoptive rearing parents had high CD scores compared to the rearing
parents with low CD scores (40.9% vs. 19.4%, χ2-test, p-value = 0.04). However, this
difference in proportions was no longer present at follow-up (IV Table 2).
The LR adoptees reared by adoptive parents with high CD scores were shown to have
a statistically significantly increased likelihood for high TDR scores at follow-up, while
no association was seen in the HR adoptees. Additional analyses of male and female
adoptees separately revealed no significant association between parents’ CD and
adoptees’ TDR at follow-up. (Table 7: IV Table 3)
48
Table 7. Association between high Communication Deviance (CD) scores of adoptive
parents at initial evaluation and likelihood for high scores in Thought Disorder Index at
follow-up among low- and high-risk adoptees in the Finnish Adoptive Family Study of
Schizophrenia (IV Table 3).
Variable LR adoptees (n=51) HR adoptees (n=38)
OR (95% CI) p-value OR (95%CI) p-value
High CD of adoptive parents 6.92 (1.30 - 36.89) 0.02 0.21 (0.02 - 2.04) 0.18
Psychiatric status (APD) 2.76 (0.56 - 13.60) 0.21 1.38 (0.22 - 8.53) 0.73
Gender, male 1.06 (0.23 - 4.81) 0.94 0.99 (0.19 - 5.06) 0.99
Age at follow-up 1.10 (0.98 - 1.23) 0.11 1.03 (0.93 - 1.14) 0.62
Social status of the adoptive 1.08 (0.23 - 5.04) 0.92 0.85 (0.17 - 4.34) 0.84
family
Note: High TDR and high CD indicate the scores belonging to upper quartile of the distribution of a variable.
6 Discussion
High scores on several TDI variables at the initial assessment predicted psychiatric
disorder at follow-up in all adoptees. These results are consistent with the previous
studies, which have suggested that thought disorder is related to psychiatric disorders
(Holzman et al. 1986, Arboleda & Holzman 1985, Solovay et al. 1987, Koistinen 1995,
Wahlberg et al. 2000). However, the early presence of any TDI variable did not alone
predict broad schizophrenia spectrum disorder at follow-up. Thus, it is very important to
recognize that elevated scores on different TDI variables can predict an increased risk to
develop any psychiatric disorders, including schizophrenia spectrum disorders. The
reason for the results obtained here could be the limited size of our sample. Only eight
cases of broad-spectrum schizophrenia were present. Prediction was statistically
unsuccessful among the high-risk (HR) adoptees because of the small number of cases,
but high scores at the 0.50 severity level did predict mental disorders among the low-risk
(LR) adoptees. However, HR adoptees did have a higher risk to have any psychiatric
diagnosis at follow-up than LR adoptees. The result is consistent with the previous
findings of the Finnish Adoptive Family Study of Schizophrenia (Tienari et al. 2000).
The 0.50 severity level had a predictive value. This result was not surprising in view
of the content of this level. The 0.50 level includes responses related to loss of mooring,
shaky reality contact, emotional overreactions, and distinct oddness (Solovay et al. 1986).
These characteristics are considered precursors of future psychosis (Olin & Mednick
1986). The absence of predictive value at the other severity levels was also logical. The
0.25 severity level responses are very general, and most people occasionally make
comments classifiable at the 0.25 level at times of fatigue or anxiety. Correspondingly,
the 0.75 severity level is in itself an obvious sign of severe psychopathology and cannot
therefore be an actually predictive sign of mental disorder.
50
Idiosyncratic verbalization was found to be related to other than broad schizophrenia
spectrum disorders. The result is in line with the findings of Holzman et al. (1986), which
showed idiosyncratic verbalization, fluid thinking, and confusion to be connected with
serious mental disorders. Surprisingly, in this study, fluid thinking and confusion did not
predict any psychiatric disorder. It was even found that the adoptees whose scores were
low on the confusion subscale tended to have some other psychiatric disorder at follow-
up, while the adoptees whose scores were high tended to have no diagnosis at all. This
result can probably be explained by the large number of 0.25 severity level responses
(word finding difficulty) on the confusion subscale in our sample. One theory is that
healthy persons’ thought processing might include such content because they might want
to achieve the best possible result in the test situation, and this might cause more
processing to choose between different words.
The number of thought disorders decreased during the follow-up period. Previous studies
have shown that, in the longitudinal perspective, age had a positive effect on, for
example, verbal ability (Schaie et al. 2004). Thus, the decrease of different TDI scores
might also be related to the maturation of thought functions. Many adoptees were quite
young (mean 25 years) at the initial assessment, and they grew up during the follow-up.
Despite the decrease of thought disorders, the main finding was that the initial TDR scores
statistically significantly predicted the TDR scores at follow-up, thus indicating the
stability of thought disorder over time. Furthermore, a more specific result was that the
stability of TDI seems to be related to the most severe categories of thought disorders.
The adoptees’ genetic or psychiatric status at follow-up did not affect the results. Thus,
genetic risk alone is probably not the only crucial factor underlying the stability of
thought disorder, but environmental factors are needed, too. This result is in the line with
the findings of Wahlberg et al. (2000), which showed idiosyncratic verbalization to be
linked not only with the genetic risk but also with the communication patterns of the
adoptive rearing parents. In our study, only genetic factors were taken into account. The
absence of stability of thought disorders among psychiatric disorders could be explained
by the low number of subjects with schizophrenia and other severe mental disorders in
our study. Marengo & Harrow (1997) especially found thought disorder to be more
prevalent and severe over time in schizophrenia than in nonschizophrenic disorders.
Episodic thought disorder is common among other psychiatric diagnoses, such as
nonpsychotic disorders (Marengo & Harrow, 1987).
An interesting gender-related result was obtained at the initial assessment. Women had
significantly more TDR scores than men. Previously studies have not addressed possible
gender differences, and the reason for this result can hence only be speculated. Yurgelun-
Todd et al. (2002) found sex-specific developmental differences in the relations between
cerebral structure and function, and it is thus possible that, in the initial test situation, the
anxiety experienced by the women was so high that it affected their thought processes.
Previous studies have shown that some psychiatric disorders, such as eating disorders,
anxiety disorders, and depression, including major depression, dysphoria, seasonal
51
affective disorder, posttraumatic stress disorder, panic disorder, and generalized anxiety
disorder, are more common among women (Strober et al. 2000). Although the possible
gender differences in the diagnoses were not investigated here, it could be speculated
whether it is possible that, in a stressful situation, the thought functions of women are
more vulnerable to confusion and more liable to thought disorders. Overall, differences in
specific cognitive functions have been found, as women have relied on emotional content
to a greater degree than men in processing information (Bremner et al. 2001).
The instability of mild thought disorders, such as 0.25 severity level responses, was
not surprising because they are related to state-like features, such as anxiety and fatigue
(Solovay et al. 1986). On the other hand, the lack of stability in fluid thinking and
confusion was rather unexpected. However, these factors are especially related to
schizophrenia, and our sample included only three subjects with schizophrenia diagnosed
at the end of the follow-up. The content of fluid thinking represents thought disorders in
which subject’s perceptions and thought processes are very unstable. Confusion also
reflects very serious vagueness and disorientation in thinking. Thus, changes in thought
disorders, which are characterized by rapid alterations, could also be very understandable.
However, it is assumed that thinking processes are cognitive qualities and hence rather
stable. In addition, the rates of occurrence of fluid thinking and confusion in our sample
were distinctly lower than that of idiosyncratic verbalization. The subjects’ maturation
could also explain the instability of fluid thinking and confusion. The adoptees grew
older during the follow-up period, and their thought processes also became less fluid and
confused. The abilities to manage stress and emotional conflicts develop later in life, and
these abilities have been found to affect the development of cognitive functions (Rowe &
Kahn 1987).
Our result on the association between the adoptees’ thought disorder and parental
Communication Deviance supported the earlier finding of Wahlberg et al. (1997).
However, adoptive parents’ CD at follow-up only predicted thought disorders in the low-
risk (LR) adoptees. It is significant that TDI scores decreased over time despite the stable
nature of thought disturbances, possibly because of the maturation of thought processes.
This phenomenon could also affect the result concerning the long-term association of CD
and TDI scores. Another explanation could be the change in the adoptees’ environment. It
is most probable that the adoptees had moved away from home during the follow-up
period. Thus, they were no longer exposed to the CD of their adoptive parents, but
possibly had a less confusing and thus more “protective” environment. Especially high-
risk (HR) adoptees have been found to be more sensitive to their environment than LR
adoptees (Wahlberg et al. 1997, Tienari et al. 2004). HR adoptees had more thought
disorder than LR adoptees if their adoptive parents had high levels of CD.
Correspondingly, HR adoptees had a lower incidence of thought disorders than LR
adoptees if they were living with low-CD adoptive parents. Thus, it could be speculated
whether the HR adoptees in this study were more sensitive to the possible positive
52
changes in their environment and therefore no longer displayed the association of TDR
with CD at follow-up.
The Finnish Adoptive Family Study of Schizophrenia is based on a study design that
provides a rare opportunity to investigate separately genetic and environmental factors,
but also to study the interaction of these variables. The most obvious strength of the
present studies is the possibility to use the unique data obtained during this adoption
study. One strength of the Finnish Adoptive Family Study of Schizophrenia is the long
follow-up time, and the present study has also taken advantage of this. In the previous
studies concerning the stability of thought disorder the follow-up periods have been
rather short (6-7 years). In our studies (II, III) the follow-up time was 11 years. The
Finnish Adoptive Family Study of Schizophrenia has also used extensive and reliable
methods. Furthermore, long follow-up data of Rorschach protocols are very rare. To our
knowledge, the Thought Disorder Index (TDI) has not been used before to assess the
stability of thought disorder in a longitudinal setting (II, III). TDI is a valid indicator of
disordered thinking in schizophrenia, and its reliability has ranged from 0.79 to 0.93.
Although the possibility to use the existing data from the Finnish Adoptive Family
Study of Schizophrenia offers many opportunities and strengths, it also poses some
limitations. First, the sample that offers the possibility to study the predictive value of
thought disorder includes only eight subjects in the broad schizophrenia spectrum group,
and the distribution of diagnoses in the group with any other psychiatric disorder was so
large that it was not possible to study which specific diagnoses the thought disorders were
related to (I). Severe mental disorders were also rare in our stability studies (II, III).
Especially the low number of schizophrenic subjects could clearly bias the results. Again,
the small number of cases in the specific diagnostic groups did not allow us to study the
putative association of different psychiatric disorders with the adoptees’ TDI level (II,
III). One further problem in our stability studies (II, III) is the fact that thought disorder
was evaluated twice. We have no way of knowing what had happened in the subjects’ life
during the follow-up time, and how the possible life events could affect the person’s
thought disorders. Furthermore, it was not possible to study reliably enough the
environmental factors in study IV. It would be especially important to know the adoptees’
place of residence during the follow-up, in order to study in more detail the high-risk
(HR) adoptees’ sensitivity to their environment (IV). The information concerning the
presence or absence of communication deviance in the environment would also be very
important. Unfortunately, the background data does not include information of the
adoptees’ place of residence. Thus, it is only possible to speculate whether or not it
affects the obtained results.
7 Conclusions
Early presence of thought disorder predicted a psychiatric disorder at follow-up (I). High
scores on TDI variables (TDR, 0.50 severity level, idiosyncratic verbalization) at the
initial assessment were found more often among the adoptees with ‘Any Psychiatric
Disorder’ (APD) at follow-up. This result was especially present among the adoptees
with ‘Any Other Psychiatric Disorder’ (AOPD). High scores at the 0.50 severity level
predicted mental disorders among the low-risk (LR) adoptees but not among the high-risk
(HR) adoptees.
The predictive value of thought disturbances is apparent, as thought disorder turned
out to be stable over time, especially in the most severe categories of thought disorder (II,
III). Stability of the TDI scores between the initial and follow-up assessments was seen at
the 0.50 and 0.75 severity levels, but not at the 0.25 severity level. Of Holzman’s
‘schizophrenia’ factors, only idiosyncratic verbalization was shown to remain stable
between the initial and follow-up assessments Again, it was shown that not only the
genotype affects thought processes. There was an association between the adoptee’s
thought disorder and the adoptive parents’ communication patterns in the longitudinal
perspective (IV). However, the adoptive parents’ CD predicted thought disorders at
follow-up only in the LR adoptees.
Numerous studies have shown the presence of thought disorder in psychiatric disorders,
especially in schizophrenia. Furthermore, previous studies have indicated that thought
disorders occur most often during the acute phase of the illness and have both trait and
state features (depending on the context). However, our results provide further evidence
of the predictive value of thought disorder. Thought disorder could be one vulnerability
sign of mental disorder,and is thus an important factor in the recognition of psychiatric
disorders. Thus, it is essential to notice that other psychiatric disorders could actually be
54
recognized much earlier than we have believed. Furthermore, this study showed that
especially severe thought disorders are not transient states but clearly have stable
features. As it is stated in the current schizophrenia care guidelines,, cognitive deficits are
common in first-episode psychosis, and it is therefore important to use
neuropsychological assessment as one element of the whole assessment procedure, in
order to recognize the high-risk subjects as early as possible (Suomen Psykiatriyhdistys,
Käypä hoito, 2001). Thus, when a person has some specific psychic symptoms, the
evaluation of thought disorder should be one tool in this assessment process. In order to
accomplish a valid and reliable assessment of thought disorder, it is advisable to have
trained psychologists elicit the Thought Disorder Index (TDI) from the Rorschach test.
It is important to remember that the presence of thought disorder is not a definitive
precursor of later mental disorder. However, it is a critical sign that should be taken
seriously, and possible interventions to clarify the individual’s thought processes should
be designed. The connection between thought disorder and parental communication
deviance in adoptive families provides ideas of how to influence the subject’s thought
processes. If thought disorder occurs, it might be useful to give appropriate information
to him/her and his/her environment (including the family) about the connection of
thought disorder and psychiatric disorders and to instruct how, in practice, to clarify the
environmental communication patterns in a such way that it helps to structure the
person’s thought processes.
Future research is especially needed to clarify the environmental factors contributing
to thought processes. A further challenge is to investigate what kind of interventions
could be appropriately used to direct the person’s cognitive development, including
thinking, into the right direction. More studies are also needed to investigate the
prevalence of thought disorders in healthy populations.
References
Adair HE & Wagner EE (1992) Stability of unusual verbalizations on the Rorschach for outpatients
with schizophrenia. Journal of Clinical Psychology 48: 250-256.
American Psychiatric Association (1987) Diagnostic and Statistical Manual of Mental Disorders.
American Psychiatric Association, Washington, DC (3rd ed., rev.).
Andreasen NJC, Tsuang MT & Canter A (1974) The significance of thought disorder in diagnostic
evaluations. Comprehensive Psychiatry 15: 27-34.
Andreasen NC. Scale for the assessment of thought, language, and communication (TLC).
Schizophrenia Bulletin. 12: 473-482.
Andreasen NC & Grove WM (1986) Thought, language, and communication in schizophrenia:
Diagnosis and prognosis. Schizophrenia Bulletin 12: 348-359.
Andreasen NC, Nopoulos P, O'Leary DS, Miller DD, Wassink T & Flaum M (1999) Defining the
phenotype of schizophrenia: cognitive dysmetria and its neural mechanisms. Biological
Psychiatry, 46: 908-920.
Arboleda C & Holzman P (1985) Thought disorder in children at risk for psychosis. Archives of
General Psychiatry 42: 1004-1013.
Arieti S (1974) Interpretation of Schizophrenia. (rev.ed.). Crosby Lockwood Staples, London.
Asarnow RF & MacCrimmon DJ (1982) Attention/information processing, neuropsychological
functioning, and thought disorder during the acute and partial recovery phases of schizophrenia:
a longitudinal study. Psychiatry Research 7: 302-319.
Asarnow JR, Goldstein MJ & Ben-Meir S (1988) Parental communication deviance in childhood
onset schizophrenia spectrum and depressive disorders. Journal of Child Psychology and
Psychiatry 29: 825-838.
Barison F (1949) Studi sul reattivo di Rorschach. I. La psicologia dei tratti e il reattivo di
Rorschach. Archivio di Psicilogia, Neurologia e Psichiatria 10: 126-156.
Bell RQ (1968) A reinterpretation of the direction of effects in studies of socialization.
Psychological Review 75: 81-95.
Benjamin M (1982) General systems theory, family systems theories, and family therapy: towards
an integrated model of family process. In: Bross A (Ed.) Family therapy. Principles of strategic
practice. The Guilford Press, New York, pp. 34-88.
Bertalanffy von L (1969) General system theory and psychiatry an overview: In: Gray W, Duhl FJ
& Rizzo ND (Eds.) General Systems Theory and Psychiatry. Little, Brown and Company,
Boston, pp. 33-50.
Bland M (1995) An Introduction to Medical Statistics. Oxford University Press, Oxford.
56
Bleuler E (1911/1950) Dementia Preacox, or the Group of Schizophrenias: Monograph Series on
Schizophrenia, No 1. International Universities Press, New York.
Bleuler E (1924) Textbook of psychiatry. MacMillan, New York.
Braff DL, Glick ID, Johnston MH & Zisook S (1988) The clinical significance of thought disorder
across time in psychiatric patients. Journal of Nervous and Mental Disorders 176: 213-220.
Bremner JD, Soufer R, McCarthy G, Delaney R, Staib LH, Duncan JS, Charney DS (2001) Gender
difference in cognitive and neural correlates of remembrance of emotional words.
Psychopharmacological Bulletin 35:55-78.
Bronfenbrenner U (1988) Interacting systems in human development: Research paradigms: present
and future. In: Bolger N, Caspi A, Downey G & Moorehouse M. Person in Context:
Developmental Process. Cambridge University Press, New York, pp. 25-49.
Bronfenbrenner U (1991a) Kognitiivisen kehityksen ekologia: tutkimusmalleja ja pakenevia
tuloksia. Osa 1. Psykologia 26: 1-15.
Bronfenbrenner U (1991b) Kognitiivisen kehityksen ekologia: tutkimusmalleja ja pakenevia
tuloksia. Osa 2. Psykologia 26: 16-28.
Cameron N (1944) Experimental analysis of schizophrenic thinking. In: Kasanin JS (ed.) Language
and Thought in Schizophrenia. Norton, New York, pp. 50-64.
Cannon, TD, Mednick SA, Parnas J, Schulsinger J, Praestholm, J. & Vestergaard A (1993)
Developmental brain abnormalities in the offspring of schizophrenic mothers. I Contributions of
genetic and perinatal factors. Archives of General Psychiatry 50: 551-564.
Cannon TD, Bearden CE, Hollister JM, Roos IM, Sanchez LE & Hadley T (2000) Childhood
cognitive functioning in schizophrenia patients and their unaffected siblings: a prospective
cohort study. Schizophrenia Bulletin 26: 379-393.
Caplan R (1994) Thought disorder in children. Journal of the American Academy of Child and
Adolescent Psychiatry 33: 605-615.
Caplan R, Guthrie D, Fish B, Tanguay PE, David-Lando G (1989) The Kiddie Formal Thought
Disorder Rating Scale (K-FTDS): clinical assessment, reliability and validity. Journal of the
American Academy of Child and Adolescent Psychiatry 28: 208-216.
Caplan R, Perdue S, Tanguay PE, Fish BE (1990) Formal thought disorder in childhood onset
schizophrenia and schizotypal personality disorder. Journal of Child Psychology and Psychiatry
31: 1103-1114.
Caplan R & Guthrie D (1992) Communication deficits in childhood schizotypal personality
disorder. Journal of American Academic Child and Adolescent Psychiatry 31: 961-967.
Caplan R, Guthrie D, Tang B, Komo S, Asarnow RF (2000) Thought disorder in childhood
schizophrenia: replication and update of concept. Journal of the American Academy of Child
Psychology and Psychiatry 39: 771-778.
Caplan R, Guthrie D, Tang B, Nuechterlein KH, Asarnow RE (2001) Thought disorder in attention-
deficit hyperactivity disorder. Journal of American Academic Child and Adolescent Psychiatry
40: 965-972.
Carpenter WT Jr & Buchanan RW (1994) Schizophrenia. New England Journal of Medicine 330:
681-690.
Carter JW, Schulsinger J, Parnas J, Cannon T & Mednick SA (2002) Multivariate prediction model
of schizophrenia. Schizophrenia Bulletin 28: 649-682.
Coleman MJ, Carpenter JT, Waternaux C, Levy DL, Shenton ME, Perry J, Medoff D, Wong H,
Monoach D, Meyer P, O’Brien C, Valentino C, Robinson D, Smith M, Makowski D &
Holzman PS (1993) The Thought Disorder Index: A Reliability Study. Psychological
Assessment 5: 336-342.
Cornblatt B, Obuchowski M, Roberts S, Pollack S & Erlenmeyer-Kimling L (1999) Cognitive and
behavioural precursors of schizophrenia. Development and Psychopathology 11: 487-508.
57
Covington MA, He C, Brown C, Naci L, McClain JT, Fjordbak BS, Semple J & Brown J (2005)
Schizophrenia and the structure of language: the linguist's view. Schizophrenia Research, 77:
85-98.
Cuesta MJ & Peralta V (1993) Does formal thought disorder differ among patients with
schizophrenic, schizophreniform and manic schizoaffective disorders? Schizophrenia Research
10: 151-158.
David AS, Malmberg A, Brandt L, Allebeck P & Lewis G (1997) IQ and risk for schizophrenia: a
population-based cohort study. Psychological Medicine 27: 1311-1323.
Davidson M, Reichenberg A, Rabinowitz J, Weiser M, Kaplan Z & Mark M (1999) Behavioral and
intellectual markers for schizophrenia in apparently healthy male adolescents. American Journal
of Psychiatry 156: 1328-1335.
Dingemans PM, Frohn-de Winter M-L, Bleeker JAC & Rathod P (1983) A cross-cultural study of
the reliability and factorial dimensions of the brief psychiatric rating scale.
Psychopharmacology 80: 190-191.
Dixon T, Kravariti E, Frith C, Murray RM & McGuire PK (2004) Effect of symptoms on executive
function in bipolar illness. Psychological Medicine 34: 811-821.
Doane JA & Rehhaut LM (1981) Communication deviance in adolescents vulnerable to subsequent
schizophrenia-spectrum disorders. Unpublished manuscript.
Doane JA, Jones JE, Fisher L, Ritzler B, Singer MT & Wynne LC (1982) Parental communication
deviance as a prediction of competence in children at risk for adult psychiatric disorder. Family
Process 21: 211-223.
Doane JA & Mintz J (1987) Communication deviance in adolescence and adulthood: A
longitudinal study. Psychiatry 50: 5-13.
Docherty NM, Cohen AS, Nienow TM, Dinzeo TJ & Dangelmaier RE (2003) Stability of formal
thought disorder and referential communication disturbances in schizophrenia. Journal of
Abnormal Psychology, 112: 469-475.
Dunayevich E & Keck PE (2000) Prevalence and description of psychotic features in bipolar
mania. Current Psychiatry Reports 2: 286-290.
Dykens E, Volkmar F & Glick M (1991) Thought disorder in high-functioning autistic adults.
Journal of Autism and Developmental Disorders 21: 291-301.
Earle-Boyer EA, Levinson JC, Grant R & Harvey PD (1986) The consistency of thought disorder
in mania and schizophrenia. II. An assessment at consecutive admissions. The Journal of
Nervous and Mental Disease 174: 443-447.
Edell WS (1987) Role of structure in disordered thinking in borderline and schizophrenic disorders.
Journal of Personality Assessment 51: 23-41.
Engel GL (1977) The need for a new medical model : a challenge for biomedicine. Science 196:
129-136.
Erkwoh R, Sabri O, Schreckenberger M, Setani K, Assfalg S, Sturz L, Fehler S & Plessmann S
(2002) Cerebral correlates of selective attention in schizophrenic patients with formal thought
disorder: a controlled H2 15O-PET study. Psychiatry Research, 115: 137-153.
Erlenmeyer-Kimling L (2001) Early neurobehavioral deficits as phenotypic indicators of the
schizophrenia genotype and predictors of later psychosis. American Journal of Medical Genetics
105: 23-24.
Erlenmeyer-Kimling L, Rock D & Roberts SA (2000) Attention, memory, and motor skills as
childhood predictors of schizophrenia-related psychoses: the New York High-Risk Project.
American Journal of Psychiatry 157: 1416-1422.
Exner JE (1993) The Rorschach: A Comprehensive System. 3rd ed. Wiley Series on Personality
Processes. Wiley, New York.
Fish FJ (1962) Schizophrenia. John Wright & Sons Ltd, Bristol.
58
Friston KJ. Imaging neuroscience: principles or maps? Proceedings of the National Academy of
Sciences of the United States of America, 95: 796-802.
Gandolfo RL, Templer DL, Cappeletty GG & Cannon WG (1991) Borderline, depressive and
schizophrenic discrimination by MMPI. Journal of Clinical Psychology 1: 181-186.
Goldberg TE, Aloia MS, Gourovitch ML, Missar D, Pickar D, Weinberger DR (1998) Cognitive
substrates of thought disorder I: the semantic system. American Journal of Psychiatry 155:
1671-1676.
Goldman-Rakic PS (1992) Working memory and the mind. Scientific American, Special Issue:
111-117.
Goldstein K (1944) Methodological approach to the study of schizophrenic thought disorder. In:
Kasanin JS (ed.) Language and Thought in Schizophrenia. Norton, New York, pp. 17-40.
Goldstein RZ, Giovannetti T, Schullery M, Zuffante PA, Lieberman JA, Robinson DG, Barr WB &
Bilder RM (2002) Neurocognitive correlates of response to treatment in formal thought disorder
in patients with first-episode schizophrenia. Neuropsychiatry, Neuropsychology, & Behavioral
Neurology, 15: 88-98.
Green MF (1998) Schizophrenia from a Neurocognitive Perspective. Probing the Impenetrable
Darkness. Allyn and Bacon, Boston.
Griner PF; Mayewski RJ, Mushlin AI & Greenland P (1981) Selection and interpretation of
diagnostic tests and procedures. Annuals of Internal Medicine 94, 555-600.
Hain C, Maier W, Hoechst-Janneck S, Franke P (1995) Subclinical thought disorder in first-degree
relatives of schizophrenia patients. Acta Psychiatrica Scandinavica 92: 305-309.
Handest P & Parnas J (2005) Clinical characteristics of first-admitted patients with ICD-10
schizotypal disorder. British Journal of Psychiatry, 48:49-54.
Handbook for Office of Statistics 17 (1983). The Center of Statistics, Helsinki.
Harrow M & Quinlan D (1977) Is disordered thinking unique to schizophrenia? Archives of
General Psychiatry 34: 15-21.
Harrow M, Grossman LS, Silverstein ML & Meltzer HY (1982) Thought pathology in manic and
schizophrenic patients: it’s occurrence at hospital admission and 7 weeks later. Archives of
General Psychiatry 39: 665-671.
Harrow M, Silverstein M & Marengo J (1983) Disordered thinking. Archives of General Psychiatry
40: 765-771.
Harrow M & Quinlan D (1985) Disordered Thinking and Schizophrenic Psychopathology. Garden
Press, New York.
Harvey PD, Docherty NM, Serper MR & Rasmussen M (1990) Cognitive deficits and thought
disorder: II. An 8-month follow-up study. Schizophrenia Bulletin 16: 147-156.
Hirayasu Y, Shenton ME, Salisbury DF, Dickey CC, Fischer IA, Mazzoni P, Kisler T, Arakaki H,
Kwon JS, Anderson JE, Yurgelun-Todd D, Tohen M & McCarley RW (1998). Lower left
temporal lobe MRI volumes in patients with first-episode schizophrenia compared with
psychotic patients with first-episode affective disorder and normal subjects. American Journal
of Psychiatry, 155: 1384-1391.
Hoffman RS, Stopek S & Andreasen NC (1986) A comparative study of manic vs. schizophrenic
speech disorganization. Archives of General Psychiatry 43: 831-838.
Holzman PS (1986) Thought disorder in schizophrenia: editor’s introduction. Schizophrenia
Bulletin 16: 147-156.
Holzman P, Shenton ME & Solovay MR (1986) Quality of thought disorder in differential
diagnosis. Schizophrenia Bulletin 12: 360-372.
Hurt SW, Holzman P & Davis JM (1983) Thought disorder: the measurement of its changes.
Archives of General Psychiatry 40: 1281-1285.
Ianzito BM, Cadoret RJ & Puch DD (1974) Thought disorder in depression. American Journal of
Psychiatry 131: 703-707.
59
Isohanni M, Jones P, Kemppainen L, Croudace T, Isohanni I, Veijola J, Räsänen S, Wahlberg K-E,
Tienari P & Rantakallio P (2000) Childhood and adolescent predictors of schizophrenia in the
Northern Finland 1966 birth cohort: a descriptive life-span model. European Archives of
Psychiatry and Clinical Neuroscience 250:1-9.
Isohanni M, Isohanni I, Koponen H, Koskinen J, Laine P, Lauronen E, Miettunen J, Maki P, Riala
K, Rasanen S, Saari K, Tienari P, Veijola J & Murray G (2004) Developmental precursors of
psychosis. Current Psychiatry Reports 6: 168-175.
Johnston MH & Holzman PS (1979) Assessing Schizophrenic Thinking. Jossey-Bass Publishers,
San Francisco.
Jones JE (1977) Patterns of transactional style deviance in the TATs of parents of schizophrenics.
Family Process 16: 327-337.
Jones JE, Rodnic EH, Goldstein MJ, McPherson SR & West KL (1977) Parental transactional style
deviance as a possible indicator of risk for schizophrenia. Archives of General Psychiatry 34:
71-74.
Jones P, Rantakallio P, Hartikainen A-L, Isohanni M, Sipilä P (1998) Schizophrenia as a long-term
outcome of pregnancy, delivery and perinatal complications: a 28 year of follow-up of the 1966
Northern Finland general population birth cohort. American Journal of Psychiatry 155: 355-364.
Jorgensen P & Aagard J (1988) Clinical predictors of course and outcome in delusional
psychosis.Acta Psychiatrica Scandinavica 77: 332-337.
Kay SR, Fiszbein A & Opler LA (1987) The positive and negative syndrome scale (PANSS) for
schizophrenia. Schizophrenia Bulletin 13: 261-276.
Kendler KS & Eaves LJ (1986) Models for the Joint Effect of Genotype and Environment on
liability to Psychiatric Illness. American Journal of Psychiatry 143: 279-289.
Kendler KS, Lieberman JA & Walsh D (1989) The Structured Interview for Schizotypy (SIS): a
preliminary report. Schizophrenia Bulletin 15: 559-571.
Kendler KS, O’Neill FA, Burke J, Murphy B, Duke F, Straub RE, Shinkwin R, Nuallain MN,
MacLean CJ & Walsh D (1996) Irish study of high-density schizophrenia families: field
methods and power to detect linkage. American Journal of Medical Genetics (Neuropsychiatric
Genetics) 67: 179-190.
Kerns JG & Berenbaum H (2003) The relationship between formal thought disorder and executive
functioning component processes. Journal of Abnormal Psychology, 112: 339-352.
Keskitalo P (2000) Stability of parental Communication Deviance and the correlation with the
development of thinking in adopted children predisposed to schizophrenia and controls. Acta
Universitatis Ouluensis D 599.
Kinney DK, Holzman PS, Jacobsen B, Jansson L, Faber B, Hildebrand W, Kasell E, Zimbalist ME
(1997) Thought disorder in schizophrenic and control adoptees and their relatives. Archives of
General Psychiatry 54: 475-479.
Kircher TT, Liddle PF, Brammer MJ, Williams SC, Murray RM & McGuire PK (2001) Neural
correlates of formal thought disorder in schizophrenia: preliminary findings from a functional
magnetic resonance imaging study. Archives of General Psychiatry, 58: 769-774.
Kircher TT, Liddle PF, Brammer MJ, Williams SC, Murray RM & McGuire PK (2002) Reversed
lateralization of temporal activation during speech production in thought disordered patients
with schizophrenia. Psychological Medicine, 32: 439-449.
Kleiger JH (1999) Disordered thinking and the Rorschach. Theory, research, and differential
diagnosis. The Analytic Press, Hillsdale NJ, London.
Kleinbaum DG (1994) Logistic regression: a self-learning text. Springer-Verlag, New York.
Klopfer B & Davidson HH (1962) The Rorschach Technique. An Introductory Manual. Harcourt,
Bruce & World, Inc, New York.
Koistinen P (1995) Thought disorder and The Rorschach. A study on psychopathology and
vulnerability of subjects. Acta Universitatis Ouluensis, Series D, Medica 346.
60
Kraepelin E (1896/1919) Dementia Preacox and Paraphrenia. E&S Livingstone, Edinburgh.
Lanin-Kettering I & Harrow M (1985) The thought behind the words: A view of schizophrenic
speech and thinking disorders. Schizophrenia Bulletin 11: 1-7.
Lee H-J, Kim Z-S & Kwon S-M (2005) Thought disorder in patients with obsessive-compulsive
disorder. Journal of Clinical Psychology, 61: 401-413.
Leeson VC, Simpson A, McKenna PJ & Laws KR (2005) Executive inhibition and semantic
association in schizophrenia. Schizophrenia Research, 74: 61-67.
Liddle PF (1987) Schizophrenic syndromes, cognitive performance, and neurologic dysfunction.
Psychological Medicine 17: 49-57.
Makowski D, Waternaux C, Lajonchere CM (1997) Thought disorder in adolescent-onset
schizophrenia. Schizophrenia research 23: 147-165.
Manschreck TC, Maher B, Celada MT, Schneyer M, Fernandez R (1991) Object chaining and
thought disorder in schizophrenic speech. Psychological Medicine 21: 443-446.
Marengo JT & Harrow M (1987) Schizophrenic Thought Disorder at Follow-up. Archives of
General Psychiatry 44: 651-659.
Marengo JT & Harrow M (1988) Thought disorder in schizophrenia. In: Tsuang MT & Simpson JC
(Eds.) Nosology, Epidemiology and Genetics of Schizophrenia. Vol. 3. Elsevier, New York, pp.
85-115.
Marengo JT & Harrow M (1997) Longitudinal courses of thought disorder in schizophrenia and
schizoaffective disorder. Schizophrenia Bulletin 23: 273-285.
McCullagh P & Nelder JA (1989) Generalized Linear Models. 2nd ed. Chapman and Hall, New
York.
McGlashan TH & Johannessen JO (1996) Early detection and intervention with schizophrenia:
rationale. Schizophrenia Bulletin 22: 201-222.
McGrath J (1991) Ordering thoughts on thought disorder. British Journal of Psychiatry 158: 307-
316.
McGorry PD, Krstev H & Harrigan S (2000) Early detection and treatment delay: implications for
outcome in early psychosis. Current Opinions in Psychiatry 13: 37-43.
McNeil TB (1991) Obstetric complications in schizophrenic patients. Schizophrenia Research 5:
89-101.
Miklowitz DJ, Velligan DI, Goldstein MJ, Nuechterlein KH, Gitlin MJ, Ranlett G & Doane JA
(1991) Communication deviance in families of schizophrenic and manic patients. Journal of
Abnormal Psychology, 100:163-173.
Miklowitz DJ & Stackman D (1992) Communication Deviance in families of schizophrenic and
other psychiatric patients: current state of the construct. In: Walker EF, Dworkin RH &
Cornblatt BA (Eds.) Experimental Personality & Psychopathology Research. Vol. 15 Springer
Publishing Company, New York, pp. 1-46.
Minassian A, Granholm E, Verney S & Perry W (2004) Pupillary dilation to simple vs. complex
tasks and its relationship to thought disturbance in schizophrenia patients. International Journal
of Psychophysiology, 52: 53-62.
Mirsky AF & Duncan CC (1986) Etiology and expression of schizophrenia: neurobiological and
psychosocial factors. Annual Review of Psychology 37: 291-319.
Monroe SM & Simons AD (1991) Diathesis-stress theories in the context of life stress research:
implications for the depressive disorders. Psychological Bulletin 110: 406-425.
Myhrman A, Rantakallio P, Isohanni M, Jones P & Partanen U (1996) Unwantedness of pregnancy
and schizophrenia in the child. British Journal of Psychiatry 169: 637-640.
Nestor PG, Shenton ME, Wible C, Hokama H, O’Donnell BF, Law S & McCarley RW (1998) A
neuropsychological analysis of schizophrenia thought disorder. Schizophrenia Research 29:
217-225.
61
Norman RM, Malla AK, Cortese L, Cheng S, Diaz K, McIntosh E, McLean TS, Rickwood A &
Voruganti LP (1999) Symptoms and cognition as predictors of community functioning: a
prospective analysis. American Journal of Psychiatry, 156: 400-405.
Nuechterlein KH & Dawson ME (1984) Information processing and attentional functioning in the
developmental course of schizophrenic disorders. Schizophrenia Bulletin 1: 160-203.
Nuechterlein KH, Edell WS, Norris M & Dawson ME (1986) Attentional vulnerability indicators,
thought disorder, and negative symptoms. Schizophrenia Bulletin 12: 408-426.
Nuechterlein KH (1987) Vulnerability models for schizophrenia. State of the art. In: Steinhauer SR,
Gruzelier JH & Zubin J (Eds), Search for the Causes of Schizophrenia. Springer-Verlag,
Giessen, p. 297-316.
Nuechterlein KH, Golstein MJ, Ventura J, Dawson ME & Doane JA (1989) Patient-environment
relationships in schizophrenia: Information processing, communication deviance, autonomic
arousal, and stressful life events. British Journal of Psychiatry 155: 84-89.
Nugter MA, Dingemanns PMAJ, Linszen DH, Van Der Does AJW & Gersons BPR (1997)
Parental communication deviance: Its stability and the effect of family treatment in recent-onset
schizophrenia. Acta Psychiatrica Scandinavica 95: 199-204.
Olin SS & Mednick SA (1986) Risk factors of psychosis: identifying vulnerable populations
premorbidly. Schizophrenia Bulletin 12: 223-240.
Ott SL, Allen J & Erlenmeyer-Kimling L (2001) The New York high-risk project: observations on
the rating of early manifestations of schizophrenia. American Journal of Medical Genetics 105:
25-27.
Ott SL, Roberts S, Rock D, Allen J & Erlenmeyer-Kimling L (2002) Positive and negative thought
disorder and psychopathology in childhood among subjects with adulthood schizophrenia.
Schizophrenia Research 58: 231-239.
Overall JE & Gorham DR (1962) The Brief Psychiatric Rating Scale. Psychological Reports 10:
799-812.
Petty RG, Barta PE, Pearlson GD, McGilchrist IK, Lewis RW, Tien AY, Pulver A, Vaughn DD,
Casanova MF & Powers RE (1995) Reversal of asymmetry of the planum temporale in
schizophrenia. American Journal of Psychiatry, 152: 715-721.
Piaget J (1988) Lapsi maailmansa rakentajana. (Kääntäjä Saara Palmgren) WSOY, Porvoo.
Pogue-Geile MF & Harrow M (1985) Negative symptoms in schizophrenia: their longitudinal
course and prognostic significance. Schizophrenia Bulletin 11: 427-439.
Ragin AB & Oltmanns TF (1986) Lexical cohesion and formal thought disorder during and after
psychotic episodes. Journal of Abnormal Psychology 95: 181-183.
Rajarethinam RP, DeQuardo JR, Nalepa R & Tandon R. Superior temporal gyrus in schizophrenia:
a volumetric magnetic resonance imaging study. Schizophrenia Research, 41: 303-312.
Rosenthal D (1963) A suggested conceptual framework. The Genain Quadruplets: A Case Study
and Theoretical Analysis of Heredity and Environment in Schizophrenia. Basic Books, New
York.
Rossi A, Serio A, Stratta P, Petruzzi C, Schiazza G, Mancini F & Casacchia M (1994) Planum
temporale asymmetry and thought disorder in schizophrenia. Schizophrenia Research, 12: 1-7.
Rubin NJ & Arceneaux JM (2001) Intractable depression or psychosis. Archives of General
Psychiatry 104: 402-405.
Rund BR (1986) Communication deviances in parents of schizophrenics. Family Process 25: 133-
147.
Sass LA, Gunderson JG, Singer MT & Wynne LC (1984) Parental communication deviance and
forms of thinking in male schizophrenic offspring. Journal of Nervous and Mental Disease 172:
513-520.
Shenton ME, Solovay MR & Holzman PS (1987) Comparative studies of thought disorders I.
Schizoaffective disorder. Archives of General Psychiatry 44: 21-30.
62
Shenton ME, Solovay MR, Holzman PS, Coleman M, Gale HJ (1989) Thought disorder in the
relatives of psychotic patients. Archives of General Psychiatry 46: 897-901.
Shenton ME, Kikinis R, Jolesz FA, Pollak SD, Lemay M, Wible CG, Hokama H, Martin J, Metcalf
D, Coleman M & McCarley RW (1992) Abnormalities of the left temporal lobe and thought
disorder in schizophrenia. New England Journal of Medicine 327: 604-612.
Simpson DL & Davies GL (1985) Measuring thought disorder with clinical rating scales in
schizophrenic and nonschizophrenic patients. Psychiatry Research 15: 313-318.
Singer M & Wynne L (1963) Differentiating characteristics of parents of childhood schizophrenics,
childhood neurotics, and young adult schizophrenics. American Journal of Psychiatry 120: 234-
243.
Singer M & Wynne L (1965a) Thought disorder and family relations of schizophrenics: III
methodology using projective techniques. Archives of General Psychiatry 12: 187-200.
Singer M & Wynne L (1965b) Thought disorder and family relations of schizophrenics. IV results
and implications. Archives of General Psychiatry 12: 201-212.
Singer MT & Wynne LC (1966) Principles for scoring communication defects and deviances in
parents of schizophrenics: Rorschach and TAT scoring manuals. Psychiatry 29: 260-288.
Singer MT, Wynne LC & Toohey ML (1978) Communication disorders and the families of
schizophrenics. In Wynne LC, Cromwell RL & Matthysse S (Eds.) The Nature of
schizophrenia. Wiley & Sons, New York.
Singer MT & Wynne LC (1986) Communication deviance scoring manual for individual
rorschachs. Unpublished manuscript.
Smith JE, Hillard MC & Roll S (1991) Rorschach evaluation of adolescent bulimics. Adolescence
23: 687-696.
Solovay MR, Shenton ME, Gasperetti C, Colleman M, Kestenbaum E, Carpenter JT & Holzman
PS (1986) Scoring manual for the Thought Disorder Index. Schizophrenia Bulletin 12:483-496.
Solovay MR, Shenton ME & Holzman PS (1987) Comparative studies of thought disorder: I. mania
and schizophrenia. Archives of General Psychiatry 44: 13-20.
Sorensen HJ, Mortensen EL, Reinisch JM & Mednick SA (2004) Association between prenatal
exposure to analgesics and risk of schizophrenia. British Journal of Psychiatry 185: 366-371.
Spitzer RL & Williams JBW (1986) Structured Clinical Interview for DSM-III-R Personality
Disorders (SCID-II). New York, New York State Psychiatric Institute, Biometrics Research.
Spitzer RL, Williams JBW & Gibbon M (1989) Structured Clinical Interview for DSM-III-R
Personality Disorders. Biometrics Research Department, New York State Psychiatric Institute,
New York.
Stierlin H (1969) Conflict and Reconciliation: A Study in Human Relations and Schizophrenia.
Doubleday, New York.
Storch A (1924) The primitive archaic forms of inner experience and thought in schizophrenia.
Nervous and Mental Disease Monographs, New York.
Strober M, Freeman R, Lampter C, Diamond J & Kaye W (2000) Controlled family study of
anorexia nervosa and bulimia nervosa: evidence of shared liability and transmission of partial
syndromes. American Journal of Psychiatry 157: 393-401.
Subotnik KL, Goldstein MJ, Nuechterlein KH, Woo SM & Mintz J (2002) Are communication
deviance and expressed emotion related to family history of psychiatric disorders in
schizophrenia? Schizophrenia Bulletin 28: 719-729.
Suomen Psykiatriyhdistys ry (Käypä hoito) (2001) Skitsofrenia. Duodecim 117: 2640-2657.
Tabachnick BG & Fidell LS (1989) Using multivariate statistics. 2nd ed., HarperCollins Publisher,
USA.
Tai S, Haddock G & Bentall R (2004) The effects of emotional salience on thought disorder in
patients with bipolar affective disorder. Psychological Medicine, 34: 803-809.
63
Tallent KA, Weinberger DR & Goldberg TE (2001) Associating semantic space abnormalities with
formal thought disorder in schizophrenia: use of triadic comparisons. Journal of Clinical &
Experimental Neuropsychology: Official Journal of the International Neuropsychological
Society, 23: 285-296.
Tienari P, Lahti I, Sorri A, Naarala M, Wahlberg K-E, Rönkkö T, Moring J & Wynne LC (1987a)
The Finnish adoptive family study of schizophrenia: possible joint effects ofgenetic
vulnerability and family interaction. In: Halweg K, Goldstein MJ (Eds.), Understanding Major
Mental disorder: The Contribution of Family Interaction Research. Family Process Press, New
York, pp.33-54.
Tienari P, Sorri A, Lahti I, Naarala M, Wahlberg K-E, Rönkkö T, Moring J, Pohjola J & Wynne
LC (1987b) Genetic and Psychosocial Factors in Schizophrenia: The Finnish Adoptive Family
Study. Schizophrenia Bulletin 13: 477-484.
Tienari P, Wynne LC, Moring J, Lahti I, Naarala M, Sorri A, Wahlberg K-E, Saarento O, Seitamaa
M, Kaleva M & Läksy K (1994) The Finnish Adoptive Study of schizophrenia: implications for
family research. British Journal of Psychiatry 164: 20-26.
Tienari P, Wynne LC, Moring J, Läksy K, Nieminen P, Sorri A, Lahti I, Wahlberg K-E, Naarala M,
Kurki-Suonio O, Koistinen P, Tarvainen T, Hakko H & Miettunen J (2000) Finnish adoptive
family study: sample selection and adoptee DSM-III-R diagnoses. Acta Psychiatrica
Scandinavica 101: 433-443.
Tienari P, Wynne LC, Läksy K (2003) Genetic Boundaries of the Schizophrenia Spectrum:
Evidence from the Finnish Adoptive Family Study. American Journal of Psychiatry 160: 1-8.
Tienari P, Wynne LC, Sorri A, Lahti I, Läksy K, Moring J, Naarala M, Nieminen P & Wahlberg K-
E (2004) Genotype-environment interaction in schizophrenia-spectrum disorder. Long-term
follow-up study of Finnish adoptees. British Journal of Psychiatry 184: 216-222.
Tochigi M, Okazaki Y, Kato N & Sasaki T (2004) What causes seasonality of birth in
schizophrenia? Neuroscience Research 48: 1-11.
Tompson MC, Asarnow JR, Hamilton EB, Newell LE, Goldstein MJ (1997) Children with
schizophrenia-spectrum disorders: thought disorder and communication problems in a family
interactional context. Journal of Child Psychology and Psychiatry 38: 421-429.
Vaever MS, Licht DM, Moller L, Perlt D, Jorgensen A, Handest P, Parnas J (2005) Thinking within
the spectrum: schizophrenic thought disorder in six Danish pedigrees. Schizophrenia Research
72: 137-149.
Van der Gaag RJ, Caplan R, van Engeland H, Loman F & Buitelaar JK (2005) A controlled study
of formal thought disorder in children with autism and multiple complex developmental
disorders. Journal of Child & Adolescent Psychopharmacology, 15:465-476.
Velligan DI, Goldstein MI & Margolin G (1988) Parental communication deviance: its relationship
to parent, child and family systems variables. Psychiatry Research 26: 313-325.
Velligan DI, Funderburg LG, Giesecke SL & Miller AL (1995) Longitudinal analysis of
communication deviance in the families of schizophrenic patients. Psychiatry 58: 6-19.
Von Domarus E (1944) The specific laws of logic in schizophrenia. In Kasanin J (ed.) Language
and Thought in Schizophrenia. University of California Press, Berkeley.
Vygotski LS (1982) Ajattelu ja kieli. (Kääntäjät K. Helkama, A. Koski-Jännes). Weilin+Göös,
Espoo.
Wagener KD, Hogarty GE, Goldstein MJ, Asarnow RF & Browne A (1986) Information
processing and communication deviance in schizophrenic patients and their mothers. Psychiatry
Research 18: 365-377.
Wahlberg K-E (1994) Parental Communication and thought disorders of offspring: an adoptive
study. Acta Universitatis Ouluensis D 305.
64
Wahlberg K-E, Wynne LC, Oja H, Keskitalo P, Pykäläinen L, Lahti I, Moring J, Naarala M, Sorri
A, Seitamaa M, Läksy K, Kolassa J & Tienari P (1997) Gene-environment interaction in
vulnerability to schizophrenia: findings from the Finnish Adoptive Family Study of schizophrenia.
American Journal of Psychiatry 154: 355-362.
Wahlberg K-E, Wynne LC, Oja H, Keskitalo P, Anias-Tanner H, Koistinen P, Tarvainen T, Hakko
H, Lahti I, Moring J, Naarala M, Sorri A & Tienari P (2000) Thought disorder index of Finnish
adoptees and communication deviance of their adoptive parents. Psychological Medicine 20:
127-136.
Wahlberg K-E, Lyman CW, Keskitalo P, Nieminen P, Moring J, Läksy K, Sorri A, Koistinen P,
Tarvainen T, Miettunen J & Tienari P (2001) Long-term stability of communication deviance.
Journal of Abnormal Psychology 110: 443-448.
Wahlberg K-E, Wynne LC, Hakko H, Läksy K, Moring J, Miettunen J & Tienari P (2004)
Interaction of genetic risk and adoptive parent communication deviance: longitudinal prediction
of adoptee psychiatric disorders. Psychological Medicine 34: 1531-1541.
Werner H (1957) The concept of development from a comparative and organismic point of view,
In: Harris DB (ed.) The Concept of Development. An Issue in the Study of Human Behavior.
University of Minnesota Press, Minneapolis, pp. 125-128.
Wilcox JA, Ramirez AL & Baida-Fragoso N (2000) The prognostic value of thought disorder in
psychotic depression. Annual Clinical Psychiatry 12: 1-4.
Wing JK, Cooper JE & Sartorius N (1974) Measurement and Classification of Psychiatric
Symptoms: An Instruction Manual for the PSE and Catego Program. Cambridge University
Press, London.
Wolff S (1991) ‘Schizoid’ personality in childhood and adult life I: the vagaries of diagnostic
labeling. British Journal of Psychiatry 159: 615-620.
Wolff S, Townshend R, Mcguire RJ, Weeks DJ (1991) ‘Schizoid’ personality in childhood and
adult life II: adult adjustment and the continuity with schizotypal personality disorder. British
Journal of Psychiatry 159: 629-635.
Wynne LC (1968) Methodologic and conceptual issues in the study of schizophrenics and their
families. Journal of Psychiatric Research 6: 185-199
Wynne LC & Singer M (1963a) Thought disorder and family relations of schizophrenics. I a
research strategy. Archives of General Psychiatry 9: 191-198.
Wynne LC & Singer M (1963b) Thought disorder and family relations of schizophrenics: II a
classification of forms of thinking. Archives of General Psychiatry 9: 199-206.
Wynne LC, Singer M, Bartko J & Toohey M (1977) Schizophrenics and their families: Recent
research on parental communication. In: Tanner JM (Ed.), Developments in psychiatric
research. Hodder & Stoughton, London.
Wynne LC (1978) From the Symptoms to Vulnerability and Beyond: An Overview: In: Wynne LC,
Cromwell RL, Matthysse S (Eds.) The Nature of Schizophrenia. New Approaches to Research
and Treatment. John Wiley & Sons, New York, pp. 698-714.
Zubin J & Spring B (1977) Vulnerability – a new view of schizophrenia. Journal of Abnormal
Psychology 86: 103-126.
Yurgelun-Todd DA, Killgore WD & Young AD (2002) Sex differences in cerebral tissue volume
and cognitive performance during adolescence. Psychological Reports 91: 743-757.
Appendix 1. The writing instructions for the Rorschach test
(these instructions are not complete)
A. Typing: The typing must be verbatim. The typist should neither “fix up” odd
statements nor distort through additions or omissions what a speaker has said. Reading
the scoring manual which follows, permits typists to see how raters willeventually
score the typescripts. The need for accurate transcribing of exact wording, word order
and reasoning becomes clear. Two main types of transcribing errors, either correcting
or distorting what a speaker actually said are to be avoided. These two problems are
discussed below.
1. Avoid fixing and correcting. Do not correct into better English, nor makeinto better
sense what is hearhd. Type without revising, substituting, or rearranging what is said
by speakers. Both beginning raters and typists should be familiar with the typing
remarks and descriptions which usually accompany viewing the Rorschach cards.
Speakers are often pointing to parts of the blots or describing features of the cards
which may be puzzling if one is not familiar with the typical exchanges which occur
during the procedure. Do not “fix” either normal ellipses, breaks in thought, nor
unusual phrasings such as illustrated below. Type what was actually said.
Here are a few examples of exact wordings, odd as they may be, which can
tempt a typist to edit, but which should be typed as heard.
I see ribs and of the esophagus.
These are protozoa, though alive they are.
A murial (sic) with outstretched arms. (i.e., mural.)
That is a carticaytchure (sic) of a man. (i.e., caricature)
To do with birth again I feel; they’re sort of uh, about to give birth itself
I think to one another.
2. Avoid distorting what is heard. If a typist faithfully avoid correcting what is heard,
only two other major problems occur; either the typing of sounds which some persons
append to words, or the failing to properly insert words which are said rapidly as a
speaker glides from one word of phrase to the next. The following examples illustrate
inclusion and omission errors:
a. Inclusion errors: Certain persons add an extra “uh” sound at the end of words
terminating in hard sounds such as “k”, “g”, “ing”, and similar sounds. These sounds
in ordinary conversation go unnoticed as part of the speaker’s regionalism or
idiosyncratic style, but are audible on tapes and are to be ignored. However, those
must be distinguished from those genuine separate “uh” sound which serve as space
fillers and non-word verbalizations, and which should be included in the typescript.
(a) Original incorrect typing of ”regionalism”: “That uh looks uh like a
dog uh with uh collar.”
(b) Correct version gained from listening to tape with knowledge about
the criteria above: “That looks like a dog, a dog with a collar”.
Inclusions such as in (a) above are not likely to be scored, but add to the work of
reading and evaluating a record. For global ratings such can mislead a reader into
thinking a speaker was extremely hesitant. The features below are likely to cause
incorrect scoring with the manual which follows this introduction.
66
b. Omissions: Failing to hear words of failing to indicate phrasing and pauses
can mislead raters.
(1) Word omissions: Short words are often elided as they are spoken.
They are formed, but faint and blended into the preceding word’s
ending or blended into the start of the following word. The
sentences below suggest a cryptic speaker:
(a) “Two figures bending forward touching something, tearing
apart”.
(b) “Here star which actually somewhat sevenpointed star”.
Rechecking the tape revealed the speaker had said many more words than a new
typist had transcribed. She had not heard the underlined words which were present in
elided form as shown here:
(a) “There are two figures bending forward touching
something and tearing it apart.”
(b) “Here’s a star, which is actually, it’s somewhat a seven-
pointed star.”
The speakers actually had fully formedand smoothly stated remarks.
(2) Phrasing omissions: A speaker groups his ideas in phrases and the
typescript should reflect accurately these groupings.
Example (a) below illustrates a failure to indicate phrasing.
Example (b) shows what checking and audiotape revealed.
(a) “Two large feet with a show with a high heel”
(b) “Two large feet with uh, shoes with a high heel”
Here a reader sees a speaker corrected his thoughts and phrased clearly whereas the
typing originally suggested one long peculiarly strung together utterance.
In summary, tapes must be checked, certain linguistic principles understood, and ideas
properly grouped until a faithful transcript of the tapes occurs.
Original publications
This thesis is based on the following original publications, which are referred to in the
text by the Roman numerals I-IV.
I Metsänen M, Wahlberg K-E, Saarento O, Tarvainen T, Miettunen J, Koistinen P,
Läksy K & Tienari P (2004) Early Presence of Thought Disorder as a Prospective
sign of Mental Disorder. Psych Res 125:193-203.
II Metsänen M, Wahlberg K-E, Saarento O, Hakko H, Tarvainen T, Koistinen P &
Tienari P (2005) Stability of Thougth Disorder Index among high-risk and low-risk
adoptees in Finnish adoptive family study of schizophrenia. Eur Psych 20:35-40.
III Metsänen M, Wahlberg K-E, Hakko H, Saarento O & Tienari P (2006) Thought
Disorder Index. A longitudinal study of severity levels and schizophrenia factors. J
Psych Res 40:258-266.
IV Metsänen M, Wahlberg K-E, Hakko H, Saarento O, Tarvainen T, Koistinen P, Tienari
P (2006) Longitudinal association between thought disorder of adoptees and
Communication Deviance of their adoptive parents. Manuscript.
The original papers have been reprinted with the permission from Elsevier (I-III).
Original publications are not included in the electronic version of the dissertation.
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Miia Metsänen
Professor Mikko Siponen
CTECHNICA
Professor Juha Kostamovaara
A STUDY OF HIGH-RISK AND LOW-RISK ADOPTEES
DMEDICA
Professor Olli Vuolteenaho
IN THE FINNISH ADOPTIVE FAMILY STUDY OF
SCHIZOPHRENIA
ESCIENTIAE RERUM SOCIALIUM
Senior Assistant Timo Latomaa
FSCRIPTA ACADEMICA
Communications Officer Elna Stjerna
GOECONOMICA
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EDITOR IN CHIEF
Professor Olli Vuolteenaho
EDITORIAL SECRETARY
Publications Editor Kirsti Nurkkala FACULTY OF MEDICINE,
DEPARTMENT OF PSYCHIATRY,
UNIVERSITY OF OULU;
ISBN 978-951-42-8331-4 (Paperback) DEPARTMENT OF PSYCHIATRY,
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